Original Article
Maternal-Fetal Disparity in HLA Class II Alloantigens and the Pregnancy-Induced Amelioration of Rheumatoid Arthritis
N Engl J Med 1993; 329:466-471August 12, 1993
- Abstract
Background
Rheumatoid arthritis frequently remits during pregnancy, for unknown reasons. Since an immune response to paternally inherited fetal HLA can occur during normal pregnancy and since rheumatoid arthritis is an autoimmune disorder with a known HLA class II antigen association, we tested the hypothesis that maternal-fetal disparity in HLA alloantigens might be associated with the pregnancy-induced remission of rheumatoid arthritis.
Methods
We studied 57 pregnancies of 41 women with rheumatoid arthritis, 18 prospectively and 39 retrospectively. Serologic and DNA techniques were used to study HLA class I and II antigens. For newborns, typing was performed from cord-blood samples obtained at delivery. For four young children, typing was performed from DNA extracted from hair samples.
Results
We found significantly more maternal-fetal disparity in HLA-DR and DQ antigens in pregnancies characterized by the remission or improvement of rheumatoid arthritis than in pregnancies characterized by active disease. Further studies using DNA-typing techniques to define allelic variants of HLA-DR and DQ antigens confirmed this observation. Maternal-fetal disparity in alleles of HLA-DRB1, DQA, and DQB occurred in 26 of 34 pregnancies characterized by remission or improvement (76 percent), as compared with 3 of 12 pregnancies characterized by active arthritis (25 percent) (odds ratio, 9.7; P = 0.003). The difference between the two groups was most marked for alleles of HLA-DQA.
Conclusions
Amelioration of rheumatoid arthritis during pregnancy is associated with a disparity in HLA class II antigens between mother and fetus. These findings suggest that the maternal immune response to paternal HLA antigens may have a role in the pregnancy-induced remission of rheumatoid arthritis.
Media in This Article
Table 1
Disparity in HLA Class I and II Antigens in Mothers with Rheumatoid Arthritis and Their Offspring, According to Whether the Arthritis Remitted or Improved during Pregnancy (Group 1) or Was Active (Group 3).Table 2
Clinical Characteristics of Women with Rheumatoid Arthritis That Remitted or Improved during Pregnancy (Group 1) and Women with Active Disease during Pregnancy (Group 3).Article Activity
- Article
Women with rheumatoid arthritis often have remissions or improvement of arthritis during pregnancy1. Although early research into the cause of this phenomenon contributed to the eventual discovery of cortisone, subsequent work showed that increased serum cortisol concentrations did not explain the improvement,2,3 and the reasons for remission remain unknown4,5.
HLA class II antigen associations have been described in many autoimmune diseases, including rheumatoid arthritis6. Why the semi-allogeneic fetus escapes rejection is an intriguing unsolved question in immunology. Pregnancy presents an immunologic challenge, and maternal immune responses to paternally inherited fetal HLA antigens occur during normal pregnancy7. Because of these observations, we tested the hypothesis that a disparity between mother and fetus in HLA class II antigens might be associated with the remission of rheumatoid arthritis during pregnancy. We determined the HLA antigens of mothers and their children and analyzed the results with respect to whether the mothers' arthritis improved during pregnancy.
Methods
Patients
We studied 57 pregnancies (39 retrospectively and 18 prospectively) in 41 women who had rheumatoid arthritis according to the 1987 revised criteria of the American Rheumatism Association8. Thirty-one of the 38 women who had undergone radiography (82 percent) had erosive changes typical of rheumatoid arthritis. In 30 of the 40 women for whom the results of tests for rheumatoid factor were available (75 percent) the results were positive. Three women for whom test results were not available were tested at study entry, when their arthritis was inactive; all were negative for rheumatoid factor. These women might have tested positive earlier in the course of their illness, since they had had severe arthritis. All study pregnancies resulted in live births. The study was approved by the institutional review committee, and informed consent was obtained from all the subjects.
Assessment of Disease Activity
Disease activity was assessed according to the patients' symptoms and use of arthritis medication and by physical examination. The women were asked to judge the activity of their arthritis on a scale from 0 (inactive) to 3 (severely active) month by month for the six months before they became pregnant, during the pregnancy, and for three months after they gave birth. In 32 of the 39 pregnancies that were studied retrospectively (82 percent), we reviewed medical records for the physicians' assessments of disease activity. The women who were studied prospectively were examined for joint pain and swelling every two to three months, and a record was kept of morning stiffness and medications taken for symptoms of arthritis.
To be included in the groups having remission (group 1A) or improvement (group 1B) during pregnancy, a woman had to have had active arthritis in the six months before pregnancy. The first four of the six criteria for remission proposed by the American Rheumatism Association9 had to be met for inclusion in group 1A, including no use of arthritis medication, no more than 15 minutes of morning stiffness each day, no joint tenderness, and no joint swelling on physical examination. The two other criteria (absence of fatigue and an erythrocyte sedimentation rate of less than 30 mm per hour) were not included in our criteria for remission, because fatigue was not thought to be a reliable symptom of arthritis in a pregnant woman and because the erythrocyte sedimentation rate rises in normal pregnant women. Our criteria for remission also required that remission be present throughout at least the final trimester of pregnancy. Once achieved, remission was sustained in all pregnancies. Twenty-two pregnancies of 21 women were included in group 1A.
The criteria for improvement (group 1B) were a reduction or discontinuation of medication, no more than 15 minutes of morning stiffness each day, improvement in joint symptoms as compared with the situation in the six months before pregnancy, and no evidence of joint swelling during the third trimester. Most women we considered to have improved satisfied all four of these criteria; those satisfying three of the four included one woman whose symptoms were the same as before pregnancy and one woman who had morning stiffness for more than 15 minutes each day in the second and third trimesters. Three women with improvement (group 1B) had more symptoms during the second trimester than during the first trimester (Patients 13, 32, and 40) and one woman (Patient 47) had palindromic symptoms during the third trimester. (This woman had also had palindromic symptoms when rheumatoid arthritis developed.) Eleven women with 12 pregnancies were included in group 1B.
Group 2 consisted of women whose rheumatoid arthritis was inactive during pregnancy but for whom it was not certain whether the disease had been active in the six months before conception. Because disease that was in remission before pregnancy and remained in remission during pregnancy might differ from active disease that remitted during pregnancy, these pregnancies were not considered in our calculations of statistical significance and were not studied with DNA typing. Group 2 included four women with 11 pregnancies.
Group 3 consisted of women who had both subjective and objective (swelling on examination) evidence of active disease during pregnancy. This group included two women (Patients 13 and 28) whose first symptoms or diagnosis was during pregnancy. Group 3 included nine women with 12 pregnancies.
In 13 of the 46 pregnancies in groups 1 and 3 (28 percent), the women had taken disease-modifying medications in the six months before pregnancy (gold, sulfasalazine, hydroxychloroquine, or methotrexate). These drugs were discontinued before pregnancy or during the first trimester, when the woman became aware of the pregnancy.
HLA Typing
Women and their children underwent HLA typing with serologic methods and sequence-specific oligonucleotide probes. Fathers were included when available (85 percent of the pregnancies in groups 1 and 3) to confirm results and to assist in the assignment of haplotypes. HLA typing of newborn infants was performed with lymphocytes isolated from cord blood at the time of delivery. In four young children, typing was performed from DNA extracted from hair samples10.
Serologic techniques detect HLA glycoprotein molecules expressed on the cell surface; the term “HLA antigen” is used to refer to these molecules. “Alloantigen” is used to refer to an HLA antigen capable of stimulating an immune response in an HLA-nonidentical subject of the same species. Each HLA molecule is composed of two polypeptide chains; in class II molecules these chains are referred to as alpha and beta chains. The DRA, DRB, DQA, and DQB genes encode the DRalpha, DRbeta, DQalpha, and DQbeta chains, respectively. Alternative forms of genes at a given genetic locus are termed alleles. DRB1, DQA, and DQB genes are polymorphic, and DNA-based sequence-specific oligonucleotide probes are used to identify the alleles for these loci.
A standard National Institutes of Health two-stage complement-dependent microcytotoxicity assay was used to define HLA-A, B, C, DR, and DQ antigens11.
Typing with Sequence-Specific Oligonucleotide Probes
DNA was prepared from peripheral-blood leukocytes, and typing with sequence-specific oligonucleotide probes for HLA-DRB1 was performed with previously described methods12,13. A panel of 11 probes was developed to detect eight alleles of HLA-DQA, including DQA*0101, *0102, *0103, *0201, *0301, *0401, *0501, and *0601; the primers were those described by Scharf et al14. HLA-DQA probes are named for amino acid polymorphisms and positions (except 27NC, a nucleotide difference not resulting in an amino acid difference) and include (by name and specificity) 52S, *0101, *0102, and *0103; 34Q, *0102, *0103, and *0501; 41K, *0103; 52H, *0201; 26S, *0301; 51L, *0401, *0501, and *0601; 75S, *0501; 25F, *0601, *0201, and *0103; 34E, *0101; 25Y, *0101, *0102, *0401, and *0501; and 75IL, *0401, *0601, and *0201. A panel of 13 probes was used to detect 13 alleles of HLA-DQB, including DQB1*0501, *0502, *0503, *0601, *0602, *0603, *0604, *0201, *0301, *0302, *0303, *0401, and *0402. The DQB probe panel was modeled on a system and used the primers described by Morel et al15. The probes were 57S, *0502; 57D, *0602 and *0603; 37D, *0601; 27NC, *0603 and *0604; 57V, *0501 and *0604; 37I, *0201; 45E, *0301; 57PD, *0301 and *0303; 57PA, *0302; 57LD, *0401 and *0402; 26GH, *0501, *0502, and *0503; 45G, *0503, *0601, *0302, *0303, *0401, and *0402; and 23L, *0401. (The sequences of the probes are available elsewhere.*) The typing systems using the HLA-DQA and DQB sequence-specific oligonucleotide probes were validated with a panel of cells for which sequencing data have been published and cells that have been studied extensively as part of international HLA workshops and for which the DQ alleles are known. The probe panels distinguish 36 possible homozygous and heterozygous combinations of HLA-DQA and all except 2 of 91 possible homozygous and heterozygous combinations of DQB.
Statistical Analysis
Twins (Patient 25) were considered as one person in the statistical analysis. The 34 pregnancies in group 1 were compared with the 12 pregnancies in group 3. The statistical methods described by Zeger and Liang16 were used because eight women in the study had two pregnancies each. Although each possible pattern of disease activity in two pregnancies in the same woman was observed, these statistical methods address the potential problem of repeated pregnancies in the same woman and incorporate a correction for the possible correlation of repeated events in a single subject. In the secondary analyses for each of the three loci, HLA-DRB1, DQA, and DQB, the Bonferroni method17 was used to correct for multiple comparisons, and statistical significance was indicated by P<0.017 rather than P<0.05.
Results
Among the 57 pregnancies in 41 women with rheumatoid arthritis, 18 were studied prospectively and 39 retrospectively. Remission of disease occurred during 22 pregnancies (group 1A), and improvement during 12 (group 1B). Arthritis was active during 12 pregnancies (group 3). There was no difference between group 1A and group 1B in the extent of HLA disparities between mother and fetus, so these two groups were combined in the analyses. The maternal-fetal disparity in HLA antigens in group 1 as compared with group 3 is shown in Table 1Table 1
Disparity in HLA Class I and II Antigens in Mothers with Rheumatoid Arthritis and Their Offspring, According to Whether the Arthritis Remitted or Improved during Pregnancy (Group 1) or Was Active (Group 3).. Disparity was examined from the perspective of the mother; it was considered to be present if a fetal HLA antigen differed from both maternal antigens, and it was considered to be absent if the fetal HLA antigen was the same as either maternal antigen. The frequency of maternal-fetal disparity in HLA-A and B antigens (class I) was similar in group 1 and group 3 (HLA-C antigens also did not differ [data not shown]). In contrast, there were more disparities between maternal and fetal class II antigens in group 1 than in group 3. There was a disparity in both HLA-DR and DQ in 76 percent of the pregnancies in group 1, as compared with 25 percent of the pregnancies in group 3 (odds ratio, 9.7; P = 0.003). There was no significant difference between the results for HLA-DR53 (DRB4) or HLA-DR52 (DRB3) in the two groups (data not shown). The results for group 2 were more similar to those for group 1 than to those for group 3, with 57 percent of the pregnancies involving disparity in HLA-DR and DQ; these results were not further analyzed, as previously explained.Previous reports18,19 found no correlation between disease activity during pregnancy and duration of disease, functional class, parity, the patient's age, or the presence of rheumatoid factor. Similarly, we found no difference between clinical factors in group 1 and group 3 (Table 2Table 2
Clinical Characteristics of Women with Rheumatoid Arthritis That Remitted or Improved during Pregnancy (Group 1) and Women with Active Disease during Pregnancy (Group 3).). These clinical factors also did not differ between pregnancies involving remission (group 1A) and those involving improvement (group 1B). The frequency of the rheumatoid arthritis susceptibility antigen HLA-DR4, previously reported to be associated with more severe disease,20,21 was similar in group 1 and group 3. Specific HLA-DRB1 susceptibility alleles for rheumatoid arthritis have been described,22 and a further association between the severity of disease and homozygosity for these alleles was recently reported23. The women were homozygous for these alleles in 12 percent of the pregnancies in which remission occurred (group 1A), as compared with 42 percent of the pregnancies in which improvement occurred (group 1B), suggesting that a maternal factor may have distinguished women who had complete remission from those whose condition only improved. In 17 percent of the pregnancies in which arthritis was active, the women were homozygous for rheumatoid arthritis susceptibility alleles.There is a wide range of allelic variation in the polymorphic DRB1, DQA, and DQB genes. Molecular techniques were therefore used to characterize further the HLA class II antigens in the study families. Disparity in HLA-DRB1, DQA, and DQB was found in 26 of the 34 pregnancies in group 1 (76 percent), as compared with 3 of the 12 pregnancies in group 3 (25 percent) (odds ratio, 9.7; P = 0.003). (The results of DNA typing are available elsewhere.NAPS) In the secondary analysis of disparity at individual loci, the odds ratio for the difference between the two groups for HLA-DRB1 was 2.8 (P = 0.28), the odds ratio for DQA was 11.6 (P = 0.002), and the odds ratio for DQB was 4.7 (P = 0.05) (Table 3Table 3
Disparity in HLA Class II Alleles between Mothers with Rheumatoid Arthritis and Their Offspring, According to Whether the Arthritis Remitted or Improved during Pregnancy (Group 1) or Was Active (Group 3).). The difference between group 1 and group 3 in HLA-DQA increased when DQA alleles were examined with respect to the number, composition, and location of differences in amino acids (Table 4Table 4
Differences in Amino Acids of HLA-DQa between Women with Rheumatoid Arthritis and Their Offspring, According to Whether the Arthritis Remitted or Improved during Pregnancy (Group 1) or Was Active (Group 3).). Only one mother and fetus in group 3 had an amino acid difference in the alpha-helical region of DQalpha24. The odds ratio for a difference in the alpha-helical region was 35.7 (P = 0.002). The increasing odds ratios for differences in HLA-DQ, DQA, and the DQA alpha-helical region (from 8.1 to 11.6 to 35.7) argue against the possibility that an unidentified gene in linkage disequilibrium is responsible for the observed association of remission with HLA-DQA. The paternally inherited fetal HLA-DRB1, DQA, and DQB alleles were diverse, and the results of an analysis of maternal disparity from the fetal perspective were nonsignificant for all loci.Two women had a remission during one pregnancy and worsening arthritis during another pregnancy. In both women, the children from the two pregnancies inherited different paternal haplotypes. One woman (Patient 38) had a remission during the first pregnancy and active disease during the second; in the first pregnancy the paternal haplotype differed for HLA-DRB1, DQA, and DQB, whereas in the second pregnancy the paternal haplotype differed for DRB1 but was identical for DQA and DQB. The second woman (Patient 48) had active disease during the first pregnancy and remission during the second; in the first pregnancy the paternal haplotype differed for HLA-DRB1 and DQB but was identical for DQA, whereas in the second pregnancy the paternal haplotype differed for DRB1, DQA, and DQB. In a third woman (Patient 13), arthritis was diagnosed during the first pregnancy and it improved during the second pregnancy. The results of this woman's first pregnancy differed from the overall study findings; although the children of both pregnancies inherited different paternal haplotypes, they both differed from the mother with regard to HLA-DRB1, DQA, and DQB.
Because of linkage disequilibrium in class II genes, the number of maternal-fetal pairs differing in only one locus was small. In just one pregnancy (Patient 47) was there isolated sharing of HLA-DQB between mother and fetus, with disparity in DRB1 and DQA. Arthritis improved in this woman, the only subject who had palindromic symptoms in the third trimester. Of the pregnancies in group 1, 12 percent involved maternal-fetal disparity in HLA-DRB1 but not DQA, as compared with 42 percent of the pregnancies in group 3. These results (in addition to the results of the secondary analysis) suggest that disparity only in HLA-DRB1 is insufficient for a favorable effect of pregnancy on rheumatoid arthritis. There was no disparity in either HLA-DRB1 or HLA-DQA in 9 percent of the pregnancies in group 1 and 33 percent of the pregnancies in group 3. Nevertheless, since 79 percent of the pregnancies in group 1 had maternal-fetal disparity in both HLA-DRB1 and HLA-DQA, as compared with 25 percent of the pregnancies in group 3, and since no mother and fetus had a disparity in DQA without a disparity in DRB1 (owing to linkage disequilibrium), DQA disparity independent of DRB1 disparity cannot be assessed. As previously shown, most of the pregnancies during which arthritis remitted or improved were characterized by fetal-maternal disparity in all three loci.
Discussion
The amelioration of rheumatoid arthritis induced by pregnancy was first described more than 50 years ago1. Improvement has been attributed to increased cortisol secretion, to sex hormones, and to a pregnancy-specific alpha-glycoprotein, but it is not likely that any of these substances are responsible2-5,25-27. We questioned whether a maternal immune response to fetal HLA antigens inherited from the father might be related to the remission of disease activity during pregnancy. In studies comparing women whose arthritis improved during pregnancy with women with active arthritis, we found that a maternal-fetal disparity in HLA class II antigens was significantly correlated with the amelioration of arthritis during pregnancy.
Trophoblastic cells do not express classic HLA antigens28. Antibodies to HLA antigens are detected in the serum of pregnant women,29-31 however, so a pregnant woman is exposed to fetal HLA antigens, either because fetal cells escape into the maternal circulation or for some other reason. Although the explanation for our findings is not known, a maternal antibody response to paternal HLA antigens represents one possibility. Antibodies to class II antigens can abrogate or modulate disease in animal models of autoimmune disease, including myasthenia gravis,32 multiple sclerosis,33 and collagen-induced arthritis34. The antibodies used in the studies of animals were directed against class II self antigens. However, clinical improvement in patients with rheumatoid arthritis has resulted from the administration of preparations of IgG immunoglobulins that were eluted from pooled human placentas35,36 and that contained alloantibodies to HLA-DR and DQ37.
In the secondary analysis among the different loci, the association of improvement in arthritis with maternal-fetal disparity in class II antigens was greater for HLA-DQ than for DR. Recent reports have demonstrated immune suppression restricted by HLA-DQ,38-40 and another explanation for our results might involve the activation of suppressor mechanisms. Since there are a number of hypotheses about the pathogenesis of autoimmunity in patients with rheumatoid arthritis, however, our results could be explained in a number of ways41. For example, HLA class II molecules, in addition to presenting foreign antigens, are also known to present self peptides. In a recent study in which peptides were eluted from mouse class II molecules and sequenced, one of the peptides eluted from the mouse I-A molecule (analogous to human DQ) was a self peptide derived from the I-Ealpha molecule (analogous to human HLA-DRalpha)42. In patients with rheumatoid arthritis, peptides derived from HLA class II molecules of the fetus might thus compete with or displace maternal self peptides according to the hypothesis that a defect in the presentation or recognition of self peptides is involved in the pathogenesis of the disease. Whatever the mechanism of remission of arthritis during pregnancy, it is likely to be complex and multifactorial. In addition, although the findings of our secondary analysis regarding HLA-DQ are intriguing, it is not possible from current studies to draw conclusions about the effect of disparity at an individual locus independent of the effect of other class II loci. Indeed, the majority of pregnancies in which remission or improvement occurred were characterized by maternal-fetal disparity in HLA-DRB1, DQA, and DQB.
In conclusion, amelioration of rheumatoid arthritis during pregnancy occurred most often when fetal and maternal HLA class II antigens differed. Further understanding of this association may provide insight into the pathogenesis of rheumatoid arthritis and possible treatment strategies.
Supported by grants from the Western Washington Arthritis Foundation and the National Institutes of Health (R29 AR39282 and AR39153) and by a Senior Investigator Award from the National Arthritis Foundation.
NAPS See NAPS document no. 05044 for three pages of supplementary material. To order, contact NAPS c/o Microfiche Publications, 248 Hempstead Tpk., West Hempstead, NY 11552.
We are indebted to the following rheumatologists and obstetricians who referred women for the study: John Baldwin, Deborah Cahill, Patrick Campbell, Frank Detraglia, John Dickson, Carin Dugowson, Gregory Gardner, Bruce Gilliland, Richard Jimenez, Michael Kennedy, James Lane, Eric Larson, John Lipani, Kenneth Mahlin, Mart Mannik, Peter Mohai, Mary Musselman, Francis Nardella, Richard Neiman, Maiz O'Conner, Ina Oppliger, Patricia Otto, Steven Overman, Scott Pollock, Eric Sasso, Peter Simkin, Wayne Tsuji, Carol Wallace, Mark Wener, Robert Willkens, and especially Jeffrey Carlin, David Wisner, and Wayne Wallis. We are indebted to Gary Longton, M.S., and Steve Self, Ph.D., for assistance with the statistical analysis, to Ms. Alison Sell for assistance in the preparation of the manuscript, and to Dr. Michael Lockshin, Dr. Daniel Geraghty, Dr. Thomas Cotner, and Dr. Patrick Beatty for review of the manuscript. The cooperation of study families, including patients, fathers, and especially young children who were willing to give blood for study purposes, is gratefully acknowledged.
Source Information
From the Human Immunogenetics Program, Division of Clinical Research, Fred Hutchinson Cancer Research Center, 1124 Columbia St., Seattle, WA 98104, where reprint requests should be addressed to Dr. Nelson.
- References
References
1
Hench PS . The ameliorating effect of pregnancy on chronic atrophic (infectious rheumatoid) arthritis, fibrositis, and intermittent hydrarthrosis. Proc Staff Meet Mayo Clinic 1938;13:161-1672
Wolfson WQ ,Robinson WD ,Duff IF . The probability that increased secretion of oxysteroids does not fully explain improvement in certain systemic diseases during pregnancy. J Mich State Med Soc 1951;50:1019-1022
Medline3
Oka M . Activity of rheumatoid arthritis and plasma 17-hydroxycorticosteroids during pregnancy and following parturition: report on two cases. Acta Rheum Scand 1958;4:243-248
Medline4
Persellin RH . The effect of pregnancy on rheumatoid arthritis. Bull Rheum Dis 1976;27:922-927
Medline5
Ostensen M ,von Schoultz B ,Husby G . Comparison between serum alpha2-pregnancy-associated globulin and activity of rheumatoid arthritis and ankylosing spondylitis during pregnancy. Scand J Rheumatol 1983;12:315-318
CrossRef | Web of Science | Medline6
Nelson JL ,Hansen JA . Autoimmune diseases and HLA. Crit Rev Immunol 1990;10:307-328[Erratum, Crit Rev Immunol 1991;10:454.]
Web of Science | Medline7
Redman CWG, Arenas J, Mason DY, Sargent IL, Sutton L. Maternal alloimmune recognition of the fetus in human pregnancy. In: Gill TJ III, Wegmann TG, eds. Immunoregulation and fetal survival. New York: Oxford University Press, 1987:210-29.
8
Arnett FC ,Edworthy SM ,Bloch DA , et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988;31:315-324
CrossRef | Web of Science | Medline9
Pinals RS ,Masi AT ,Larsen RA , et al. Preliminary criteria for clinical remission in rheumatoid arthritis. Arthritis Rheum 1981;24:1308-1315
CrossRef | Web of Science | Medline10
von Beroldingen CH, Blake ET, Iguchi R, Sensbaugh GF, Erlich HA. Applications of PCR to analysis of biological evidence. In: Erlich HA, ed. PCR technology: principles and applications for DNA amplification. New York: Stockton Press, 1989:209-23.
11
NIH lymphocyte microcytotoxicity technique. In: Ray JG Jr, ed. NIAID manual of tissue typing techniques: 1979-1980. Bethesda, Md.: National Institutes of Health, 1979:39-41. (NIH publication no. 80-545.)
12
Petersdorf EW ,Smith AG ,Mickelson EM ,Martin PJ ,Hansen JA . Ten HLA-DR4 alleles defined by sequence polymorphisms within the DRB1 first domain. Immunogenetics 1991;33:267-275
CrossRef | Web of Science | Medline13
Petersdorf EW ,Smith AG ,Haase AM ,Martin PJ ,Hansen JA . Polymorphism of HLA-DRw52-associated DRB1 genes as defined by sequence-specific oligonucleotide probe hybridization and sequencing. Tissue Antigens 1991;38:169-177
CrossRef | Web of Science | Medline14
Scharf SJ ,Horn GT ,Erlich HA . Direct cloning and sequence analysis of enzymatically amplified genomic sequences. Science 1986;233:1076-1078
CrossRef | Web of Science | Medline15
Morel C ,Zwahlen F ,Jeannet M ,Mach B ,Tiercy JM . Complete analysis of HLA-DQB1 and DR-DQ linkage disequilibrium by oligonucleotide typing. Hum Immunol 1990;29:64-77
CrossRef | Web of Science | Medline16
Zeger SL ,Liang K-Y . Longitudinal data analysis for discrete and continuous outcomes. Biometrics 1986;42:121-130
CrossRef | Web of Science | Medline17
Miller RG Jr. Simultaneous statistical inference. 2nd ed. Springer series in statistics. New York: Springer-Verlag, 1981.
18
Neely NT ,Persellin RH . Activity of rheumatoid arthritis during pregnancy. Tex Med 1977;73:59-63
Medline19
Ostensen M ,Husby G . A prospective clinical study of the effect of pregnancy on rheumatoid arthritis and ankylosing spondylitis. Arthritis Rheum 1983;26:1155-1159
CrossRef | Web of Science | Medline20
van Zeben D ,Hazes JM ,Zwinderman AH , et al. Association of HLA-DR4 with a more progressive disease course in patients with rheumatoid arthritis: results of a followup study. Arthritis Rheum 1991;34:822-830
CrossRef | Web of Science | Medline21
Calin A ,Elswood J ,Klouda P . Destructive arthritis, rheumatoid factor, and HLA-DR4: susceptibility versus severity, a case-control study. Arthritis Rheum 1989;32:1221-1225
CrossRef | Web of Science | Medline22
Winchester R ,Dwyer E ,Rose S . The genetic basis of rheumatoid arthritis: the shared epitope hypothesis. Rheum Dis Clin North Am 1992;18:761-783
Web of Science | Medline23
Weyand CM ,Hicok KC ,Conn DL ,Goronzy JJ . The influence of HLA-DRB1 genes on disease severity in rheumatoid arthritis. Ann Intern Med 1992;117:801-806
Web of Science | Medline24
Brown JH ,Jardetzky T ,Saper MA ,Samraoui B ,Bjorkman PJ ,Wiley DC . A hypothetical model of the foreign antigen binding site of class II histocompatibility molecules. Nature 1988;332:845-850[Erratum, Nature 1988;333:786.]
CrossRef | Web of Science | Medline25
Gilbert M ,Rotstein J ,Cunningham C ,Estrin I ,Davidson A ,Pincus G . Norethynodrel with mestranol in treatment of rheumatoid arthritis. JAMA 1964;190:235-235
Web of Science | Medline26
Persellin RH ,Wiginton DAF ,Rutstein JE , et al. Pregnancy alpha-glycoprotein (PAG) and rheumatoid arthritis (RA) activity: a prospective analysis during gestation. Arthritis Rheum 1982;25:Suppl:S6-S6 abstract.
CrossRef | Web of Science27
Bijlsma JWJ ,van den Brink HR . Estrogens and rheumatoid arthritis. Am J Reprod Immunol 1992;28:231-234
Web of Science | Medline28
Loke YW ,King A . Recent developments in the human maternal-fetal immune interaction. Curr Opin Immunol 1991;3:762-766
CrossRef | Web of Science | Medline29
Payne R . Leukocyte agglutinins in human sera: correlation between blood transfusions and their development. Arch Intern Med 1957;99:587-606
Web of Science30
Morin-Papunen L ,Tiilikainen A ,Hartikainen-Sorri A-L . Maternal HLA immunization during pregnancy: presence of anti HLA antibodies in half of multigravidous women. Med Biol 1984;62:323-325
Medline31
Suciu-Foca N ,Reed E ,Rohowsky C ,Kung P ,King DW . Anti-idiotypic antibodies to anti-HLA receptors induced by pregnancy. Proc Natl Acad Sci U S A 1983;80:830-834
CrossRef | Web of Science | Medline32
Waldor MK ,Sriram S ,McDevitt HO ,Steinman L . In vivo therapy with monoclonal anti-I-A antibody suppresses immune responses to acetylcholine receptor. Proc Natl Acad Sci U S A 1983;80:2713-2717
CrossRef | Web of Science | Medline33
Steinman L ,Rosenbaum JT ,Sriram S ,McDevitt HO . In vivo effects of antibodies to immune response gene products: prevention of experimental allergic encephalitis. Proc Natl Acad Sci U S A 1981;78:7111-7114
CrossRef | Web of Science | Medline34
Wooley PH ,Luthra HS ,Lafuse WP ,Huse A ,Stuart JM ,David CWS . Type II collagen-induced arthritis in mice. III. Suppression of arthritis by using monoclonal and polyclonal anti-Ia antisera. J Immunol 1985;134:2366-2374
Web of Science | Medline35
Sany J ,Clot J ,Bonneau M ,Andary M . Immunomodulating effect of human placenta-eluted gamma globulins in rheumatoid arthritis. Arthritis Rheum 1982;25:17-24
CrossRef | Web of Science | Medline36
Combe B ,Cosso B ,Clot J ,Bonneau M ,Sany J . Human placenta-eluted gammaglobulins in immunomodulating treatment of rheumatoid arthritis. Am J Med 1985;78:920-928
CrossRef | Web of Science | Medline37
Moynier M ,Cosso B ,Brochier J ,Clot J . Identification of class II HLA alloantibodies in placenta-eluted gamma globulins used for treating rheumatoid arthritis. Arthritis Rheum 1987;30:375-381
CrossRef | Web of Science | Medline38
Salgame P ,Convit J ,Bloom BR . Immunological suppression by human CD8+ T cells is receptor dependent and HLA-DQ restricted. Proc Natl Acad Sci U S A 1991;88:2598-2602
CrossRef | Web of Science | Medline39
Nishimura Y ,Sasazuki T . Suppressor T cells control the HLA-linked low responsiveness to streptococcal antigen in man. Nature 1983;302:67-69
CrossRef | Web of Science | Medline40
Ottenhoff THM ,Elferink DG ,Klatser PR ,de Vries RRP . Cloned suppressor T cells from a lepromatous leprosy patient suppress Mycobacterium leprae reactive helper T cells. Nature 1986;322:462-464
CrossRef | Web of Science | Medline41
Harris ED Jr . Rheumatoid arthritis: pathophysiology and implications for therapy. N Engl J Med 1990;322:1277-1289
Full Text | Web of Science | Medline42
Rudensky AY ,Preston-Hurlburt P ,Hong S-C ,Barlow A ,Janeway CA Jr . Sequence analysis of peptides bound to MHC class II molecules. Nature 1991;353:622-627
CrossRef | Web of Science | Medline
- Citing Articles (112)
Citing Articles
1
May Ching Soh, Catherine Nelson-Piercy. (2012) Update of the management of rheumatoid arthritis in pregnancy. Expert Review of Obstetrics & Gynecology 7:1, 77-96
CrossRef2
Monika Østensen, Peter M. Villiger, Frauke Förger. (2011) Interaction of pregnancy and autoimmune rheumatic disease. Autoimmunity Reviews
CrossRef3
J. M. W. Hazes, P. G. Coulie, V. Geenen, S. Vermeire, F. Carbonnel, E. Louis, P. Masson, F. De Keyser. (2011) Rheumatoid arthritis and pregnancy: evolution of disease activity and pathophysiological considerations for drug use. Rheumatology 50:11, 1955-1968
CrossRef4
S. Scherjon, L. Lashley, M.-L. van der Hoorn, F. Claas. (2011) Fetus specific T cell modulation during fertilization, implantation and pregnancy. Placenta 32, S291-S297
CrossRef5
Shreyasee Amin, Erik J. Peterson, Ann M. Reed, Daniel L. Mueller. (2011) Pregnancy and Rheumatoid Arthritis: Insights into the Immunology of Fetal Tolerance and Control of Autoimmunity. Current Rheumatology Reports 13:5, 449-455
CrossRef6
Alba Munoz-Suano, Marinos Kallikourdis, Milka Sarris, Alexander G. Betz. (2011) Regulatory T cells protect from autoimmune arthritis during pregnancy. Journal of Autoimmunity
CrossRef7
Erardo Meriño-Ibarra, Concepción Delgado Beltrán. (2011) Artritis reumatoide: ¿cómo usar los fármacos en el embarazo y la lactancia?. Reumatología Clínica 7:4, 262-266
CrossRef8
Norbert Gleicher, Andrea Weghofer, David H. Barad. (2011) Cutting edge assessment of the impact of autoimmunity on female reproductive success. Journal of Autoimmunity
CrossRef9
Norbert Gleicher, David H. Barad. (2011) Gestational Dermatosis Shortly after Implantation Associated with Parental Class II HLA Compatibility and Maternal Immune Activation: Preliminary Report of a Prospective Case Series. Dermatology 222:3, 206-211
CrossRef10
Erardo Meriño-Ibarra, Concepción Delgado Beltrán. (2011) Rheumatoid arthritis: How to use drugs during pregnancy and lactation?. Reumatolog ía Cl ínica (English Edition) 7:4, 262-266
CrossRef11
Norbert Gleicher. (2010) Does the Immune System Induce Labor? Lessons from Preterm Deliveries in Women with Autoimmune Diseases. Clinical Reviews in Allergy & Immunology 39:3, 194-206
CrossRef12
Gyula Richárd Nagy, Bence Péter Neducsin, János Rigó .. (2010) Microchimaerismus mint terhességi örökség. Orvosi Hetilap 151:49, 2019-2024
CrossRef13
E. F. Chakravarty. (2010) Rheumatoid arthritis and pregnancy: where do we go from here?. Journal of Internal Medicine 268:4, 309-311
CrossRef14
Lola Y Kwan, Uma Mahadevan. (2010) Inflammatory bowel disease and pregnancy: an update. Expert Review of Clinical Immunology 6:4, 643-657
CrossRef15
K Mitchell, M Kaul, MEB Clowse. (2010) The management of rheumatic diseases in pregnancy. Scandinavian Journal of Rheumatology 39:2, 99-108
CrossRef16
Saoussen Hassen Zrour, Radia Boumiza, Nabil Sakly, Rim Mannai, Wided Korbaa, Mohamed Younes, Ismail Bejia, Mongi Touzi, Naceur Bergaoui. (2010) The impact of pregnancy on rheumatoid arthritis outcome: The role of maternofetal HLA class II disparity. Joint Bone Spine 77:1, 36-40
CrossRef17
Osamu SAMURA. (2010) Fetal microchimerism and autoimmune disease. Japanese Journal of Clinical Immunology 33:6, 293-303
CrossRef18
Uma Mahadevan. (2010) Pregnancy and Inflammatory Bowel Disease. Medical Clinics of North America 94:1, 53-73
CrossRef19
Lisa R. Sammaritano. 2010. Management of the Patient with Rheumatic Disease During and After Pregnancy. , 420-439.
CrossRef20
Uma Mahadevan. (2009) Pregnancy and Inflammatory Bowel Disease. Gastroenterology Clinics of North America 38:4, 629-649
CrossRef21
Norbert Gleicher, Uri Elkayam. (2009) Peripartum cardiomyopathy, an autoimmune manifestation of allograft rejection?. Autoimmunity Reviews 8:5, 384-387
CrossRef22
Lori A. Lavelle, William F. Lavelle, Elizabeth Demers Lavelle. 2009. RHEUMATOID ARTHRITIS. , 245-250.
CrossRef23
Megan EB Clowse. (2008) Impact of pregnancy on rheumatoid arthritis activity. Future Rheumatology 3:6, 527-531
CrossRef24
Marla Dubinsky, Bincy Abraham, Uma Mahadevan. (2008) Management of the pregnant IBD patient. Inflammatory Bowel Diseases 14:12, 1736-1750
CrossRef25
Anne L. Dunlop, Brian W. Jack, Joseph N. Bottalico, Michael C. Lu, Andra James, Cynthia S. Shellhaas, Lynne Haygood-Kane Hallstrom, Benjamin D. Solomon, W. Gregory Feero, M. Kathryn Menard, Mona R. Prasad. (2008) The clinical content of preconception care: women with chronic medical conditions. American Journal of Obstetrics and Gynecology 199:6, S310-S327
CrossRef26
Yaël A. de Man, Radboud J. E. M. Dolhain, Fleur E. van de Geijn, Sten P. Willemsen, Johanna M. W. Hazes. (2008) Disease activity of rheumatoid arthritis during pregnancy: Results from a nationwide prospective study. Arthritis & Rheumatism 59:9, 1241-1248
CrossRef27
Shu Kobayashi, Shigeki Momohara, Naoyuki Kamatani, Hiroshi Okamoto. (2008) Molecular aspects of rheumatoid arthritis: role of environmental factors. FEBS Journal 275:18, 4456-4462
CrossRef28
Norbert Gleicher. (2008) Graft-versus-host disease and immunologic rejection: implications for diagnosis and treatments of pregnancy complications. Expert Review of Obstetrics & Gynecology 3:1, 37-49
CrossRef29
Norbert Gleicher. (2008) Missed immunological opportunities in pregnancy. Expert Review of Clinical Immunology 4:1, 1-3
CrossRef30
Leslie Cleland, Lisa Stamp. 2007. Rheumatoid Arthritis. .
CrossRef31
Norbert Gleicher. (2007) Postpartum depression, an autoimmune disease?. Autoimmunity Reviews 6:8, 572-576
CrossRef32
Yaël A. de Man, Johanna M. W. Hazes, Fleur E. van de Geijn, Catharina Krommenhoek, Radboud J. E. M. Dolhain. (2007) Measuring disease activity and functionality during pregnancy in patients with rheumatoid arthritis. Arthritis & Rheumatism 57:5, 716-722
CrossRef33
Monika Østensen, Peter M. Villiger. (2007) The remission of rheumatoid arthritis during pregnancy. Seminars in Immunopathology 29:2, 185-191
CrossRef34
K.M. Adams, Z. Yan, A.M. Stevens, J.L. Nelson. (2007) The Changing Maternal “Self” Hypothesis: A Mechanism for Maternal Tolerance of the Fetus. Placenta 28:5-6, 378-382
CrossRef35
Norbert Gleicher. (2007) Pregnancy-related cell traffic, microchimerism and autoimmunity: the possibility of reducing autoimmune disease prevalence. Expert Review of Obstetrics & Gynecology 2:3, 341-345
CrossRef36
John M Cafardi, Graciela S Alarcón, Kenneth G Saag. (2007) Effect of reproductive factors on rheumatoid arthritis. Future Rheumatology 2:2, 177-183
CrossRef37
Evangelos Cholongitas, George V. Papatheodoridis, Paola Zappoli, Athanasios Giannakopoulos, David Patch, Laura Marelli, Vibhakorn Shusang, George Kalambokis, Graham Shirling, Nancy Rolando, A. K. Burroughs. (2007) Combined HLA-DR and -DQ disparity is associated with a stable course of ulcerative colitis after liver transplantation for primary sclerosing cholangitis. Liver Transplantation 13:4, 552-557
CrossRef38
Norbert Gleicher. (2007) Why much of the pathophysiology of preeclampsia-eclampsia must be of an autoimmune nature. American Journal of Obstetrics and Gynecology 196:1, 5.e1-5.e7
CrossRef39
Camilla Drexler, Thomas Wagner. (2006) Blood group chimerism. Current Opinion in Hematology 13:6, 484-489
CrossRef40
Andrea Doria, Luca Iaccarino, Silvia Arienti, Anna Ghirardello, Sandra Zampieri, Maria Elisa Rampudda, Maurizio Cutolo, Angela Tincani, Silvano Todesco. (2006) Th2 immune deviation induced by pregnancy: The two faces of autoimmune rheumatic diseases. Reproductive Toxicology 22:2, 234-241
CrossRef41
Zhen Yan, Nathalie C. Lambert, Monika ØStensen, Kristina M. Adams, Katherine A. Guthrie, J. Lee Nelson. (2006) Prospective study of fetal DNA in serum and disease activity during pregnancy in women with inflammatory arthritis. Arthritis & Rheumatism 54:7, 2069-2073
CrossRef42
E. Gromnica-Ihle, M. Østensen. (2006) Schwangerschaft bei rheumatoider Arthritis oder Spondyloarthritiden. Zeitschrift für Rheumatologie 65:3, 209-216
CrossRef43
Liliana Candia, Javier Marquez, Luis R. Espinoza. (2005) Autoimmune Hepatitis and Pregnancy: A Rheumatologist's Dilemma. Seminars in Arthritis and Rheumatism 35:1, 49-56
CrossRef44
Thomas Vauvert F. Hviid, Ole B. Christiansen. (2005) Linkage Disequilibrium Between Human Leukocyte Antigen (HLA) Class II and HLA-G—Possible Implications for Human Reproduction and Autoimmune Disease. Human Immunology 66:6, 688-699
CrossRef45
M.E. Mullarkey, A.M. Stevens, W.M. McDonnell, L.S. Loubiere, J.A. Brackensick, J.M. Pang, A.J. Porter, D.A. Galloway, J.L. Nelson. (2005) Human leukocyte antigen class II alleles in Caucasian women with primary biliary cirrhosis. Tissue Antigens 65:2, 199-205
CrossRef46
Sunanda Kane, John Kisiel, Lorena Shih, Stephen Hanauer. (2004) HLA Disparity Determines Disease Activity through Pregnancy in Women with Inflammatory Bowel Disease. The American Journal of Gastroenterology 99:8, 1523-1526
CrossRef47
Takao Ando, Terry F Davies. (2004) Self-recognition and the role of fetal microchimerism. Best Practice & Research Clinical Endocrinology & Metabolism 18:2, 197-211
CrossRef48
Nathalie C. Lambert, Timothy D. Erickson, Zhen Yan, Jennifer M. Pang, Katherine A. Guthrie, Daniel E. Furst, J. Lee Nelson. (2004) Quantification of maternal microchimerism by HLA-specific real-time polymerase chain reaction: Studies of healthy women and women with scleroderma. Arthritis & Rheumatism 50:3, 906-914
CrossRef49
Karen M. Palaszynski, Kyi Kyi Loo, Judith F. Ashouri, Hong-biao Liu, Rhonda R. Voskuhl. (2004) Androgens are protective in experimental autoimmune encephalomyelitis: implications for multiple sclerosis. Journal of Neuroimmunology 146:1-2, 144-152
CrossRef50
Ann M. Reed. (2003) Microchimerism in children with rheumatic disorders: What does it mean?. Current Rheumatology Reports 5:6, 458-462
CrossRef51
Suraksha Agrawal, Manoj Kumar Pandey. (2003) The Potential Role of HLA-G Polymorphism in Maternal Tolerance to the Developing Fetus. Journal of Hematotherapy <html_ent glyph="@amp;" ascii="&"/> Stem Cell Research 12:6, 749-756
CrossRef52
Ann M. Reed. (2003) Chimerism in myositis. Current Rheumatology Reports 5:6, 421-424
CrossRef53
Linda A Merlino, James R Cerhan, Lindsey A Criswell, Ted R Mikuls, Kenneth G Saag. (2003) Estrogen and other female reproductive risk factors are not strongly associated with the development of rheumatoid arthritis in elderly women. Seminars in Arthritis and Rheumatism 33:2, 72-82
CrossRef54
Peter K Rabiah, Albert T Vitale. (2003) Noninfectious uveitis and pregnancy. American Journal of Ophthalmology 136:1, 91-98
CrossRef55
Hanns Kaiser. (2003) Cortisontherapie heute. Wiener Klinische Wochenschrift 115:1-2, 6-21
CrossRef56
Monika Østensen, Peter M Villiger. (2002) Immunology of pregnancy—pregnancy as a remission inducing agent in rheumatoid arthritis. Transplant Immunology 9:2-4, 155-160
CrossRef57
J. Lee Nelson. (2002) Pregnancy and microchimerism in autoimmune disease: Protector or insurgent?. Arthritis & Rheumatism 46:2, 291-297
CrossRef58
Francis J. Keefe, Suzanne J. Smith, Angela L. H. Buffington, Jessica Gibson, Jamie L. Studts, David S. Caldwell. (2002) Recent advances and future directions in the biopsychosocial assessment and treatment of arthritis.. Journal of Consulting and Clinical Psychology 70:3, 640-655
CrossRef59
Hiromichi Ariga, Hitoshi Ohto, Michael P. Busch, Shinya Imamura, Robert Watson, William Reed, Tzong-Hae Lee. (2001) Kinetics of fetal cellular and cell-free DNA in the maternal circulation during and after pregnancy: implications for noninvasive prenatal diagnosis. Transfusion 41:12, 1524-1530
CrossRef60
Nisar A Khan, Afshan Khan, Huub F.J Savelkoul, Robbert Benner. (2001) Inhibition of diabetes in NOD mice by human pregnancy factor. Human Immunology 62:12, 1315-1323
CrossRef61
J.Lee Nelson. (2001) HLA relationships of pregnancy, microchimerism and autoimmune disease. Journal of Reproductive Immunology 52:1-2, 77-84
CrossRef62
N. C. LAMBERT, A. M. STEVENS, T. S. TYLEE, T. D. ERICKSON, D. E. FURST, J. L. NELSON. (2001) From the Simple Detection of Microchimerism in Patients with Autoimmune Diseases to Its Implication in Pathogenesis. Annals of the New York Academy of Sciences 945:1, 164-171
CrossRef63
J. Lee Nelson. (2001) Microchimerism and hla relationships of pregnancy: Implications for autoimmune diseases. Current Rheumatology Reports 3:3, 222-229
CrossRef64
J Lee Nelson, Nathalie C Lambert. (2001) Microchimerism in rheumatic diseases. Joint Bone Spine 68:4, 290-296
CrossRef65
M. Imaizumi, A. Pritsker, M. Kita, L. Ahmad, P. Unger, T. F. Davies. (2001) Non-MHC Driven Exacerbation of Experimental Thyroiditis in the Postpartum Period. Autoimmunity 34:2, 95-105
CrossRef66
Keith S. Kanik, Ronald L. Wilder. (2000) HORMONAL ALTERATIONS IN RHEUMATOID ARTHRITIS, INCLUDING THE EFFECTS OF PREGNANCY. Rheumatic Disease Clinics of North America 26:4, 805-823
CrossRef67
Ajay K. Singh. (2000) Lupus nephritis and the anti-phospholipid antibody syndrome in pregnancy. Kidney International 58:5, 2240-2254
CrossRef68
Alfonse T. Masi, Johannes W.J. Bijlsma, Ian C. Chikanza, Constantino Pitzalis, Maurizio Cutolo. (1999) Neuroendocrine, immunologic, and microvascular systems interactions in rheumatoid arthritis: physiopathogenetic and therapeutic perspectives. Seminars in Arthritis and Rheumatism 29:2, 65-81
CrossRef69
URSZULA S. MASIUKIEWICZ, GERARD N. BURROW. (1999) Hyperthyroidism in Pregnancy: Diagnosis and Treatment. Thyroid 9:7, 647-652
CrossRef70
TERRY F. DAVIES. (1999) The Thyroid Immunology of the Postpartum Period. Thyroid 9:7, 675-684
CrossRef71
Sean Maloney, Anajane Smith, Daniel E. Furst, David Myerson, Kate Rupert, Paul C. Evans, J. Lee Nelson. (1999) Microchimerism of maternal origin persists into adult life. Journal of Clinical Investigation 104:1, 41-47
CrossRef72
RONALD L. WILDER, ILIA J. ELENKOV. (1999) Hormonal Regulation of Tumor Necrosis Factor-alpha, Interleukin-12 and Interleukin-10 Production by Activated Macrophages: A Disease-modifying Mechanism in Rheumatoid Arthritis and Systemic Lupus Erythematosus?. Annals of the New York Academy of Sciences 876:1 NEUROENDOCRIN, 14-31
CrossRef73
Jennifer H. Barrett, Paul Brennan, Magdalen Fiddler, Alan J. Silman. (1999) Does rheumatoid arthritis remit during pregnancy and relapse postpartum?: Results from a nationwide study in the United Kingdom performed prospectively from late pregnancy. Arthritis & Rheumatism 42:6, 1219-1227
CrossRef74
J. Lee Nelson. (1999) Microchimerism and scleroderma. Current Rheumatology Reports 1:1, 15-21
CrossRef75
MONICA OSTENSEN. (1999) Sex Hormones and Pregnancy in Rheumatoid Arthritis and Systemic Lupus Erythematosus. Annals of the New York Academy of Sciences 876:1 NEUROENDOCRIN, 131-144
CrossRef76
Janet E. Pope, Nicholas Bellamy, Adam Stevens. (1999) The lack of associations between rheumatoid arthritisand both nulliparity and infertility. Seminars in Arthritis and Rheumatism 28:5, 342-350
CrossRef77
Julie L. Rosen, Huy T. Tran, Alan Lackey, Susan M. Viselli. (1999) Sex-Related Immune Changes in Young Mice. Immunological Investigations 28:4, 247-256
CrossRef78
Warner, Jones, Williams, Warner. (1998) Maternal programming in asthma and allergy. Clinical <html_ent glyph="@amp;" ascii="&"/> Experimental Allergy 28:Suppl. 5, 35-38
CrossRef79
RONALD L. WILDER. (1998) Hormones, Pregnancy, and Autoimmune Diseases. Annals of the New York Academy of Sciences 840:1 NEUROIMMUNOMO, 45-50
CrossRef80
J Lee Nelson, Daniel E Furst, Sean Maloney, Ted Gooley, Paul C Evans, Anajane Smith, Michael A Bean, Carole Ober, Diana W Bianchi. (1998) Microchimerism and HLA-compatible relationships of pregnancy in scleroderma. The Lancet 351:9102, 559-562
CrossRef81
Carole Ober. (1998) HLA and Pregnancy: The Paradox of the Fetal Allograft. The American Journal of Human Genetics 62:1, 1-5
CrossRef82
Elise Belilos, Steven Carsons. (1998) RHEUMATOLOGIC DISORDERS IN WOMEN. Medical Clinics of North America 82:1, 77-101
CrossRef83
Pierre Miossec, Wim Van Den Berg. (1997) Th1/Th2 cytokine balance in arthritis. Arthritis & Rheumatism 40:12, 2105-2115
CrossRef84
Mark K. Haynes, J.Bruce Smith. (1997) Can Th1-like immune responses explain the immunopathology of recurrent spontaneous miscarriage?. Journal of Reproductive Immunology 35:1, 65-71
CrossRef85
G.P. Russwurm, A.M. Mackler, O.R. Fagoaga, W.S. Brown, E.P. Sakala, S.M. Yellon, S.L. Nehlsen-Cannarella. (1997) Soluble Human Leukocyte Antigens, Interleukin-6, and Interferon-γ During Pregnancy. American Journal of Reproductive Immunology 38:4, 256-262
CrossRef86
Denise M. Damek, Elizabeth A. Shuster. (1997) Pregnancy and Multiple Sclerosis. Mayo Clinic Proceedings 72:10, 977-989
CrossRef87
Magdalen A. Fiddler. (1997) Rheumatoid arthritis and pregnancy: Issues for consideration in clinical management. Arthritis Care & Research 10:4, 264-272
CrossRef88
Sachiko Miyagawa, Takaya Fukumoto, Kazuko Hashimoto, Akira Yoshioka, Toshihiko Shirai, Koji Shinohara, Kin-Ichi Kidoguchi, Tomio Fujita. (1997) Neonatal lupus erythematosus: Haplotypic analysis of HLA class II alleles in child/mother pairs. Arthritis & Rheumatism 40:5, 982-983
CrossRef89
Larry W. Moreland, Louis W. Heck, William J. Koopman. (1997) Biologic agents for treating rheumatoid arthritis. Concepts and progress. Arthritis & Rheumatism 40:3, 397-409
CrossRef90
JULIETTE TRANCHOT-DIALLO, GABRIEL GRAS, OLIVIER BENVENISTE, DOMINIQUE MARCÉ, PIERRE ROQUES, DOMINIQUE DORMONT, FRANÇOISE PARNET-MATHIEU, JACQUES MILLIEZ, GÉRARD CHAOUAT. (1997) Modulations of Cytokine Expression in Pregnant Women. American Journal of Reproductive Immunology 37:3, 215-226
CrossRef91
J. Lee Nelson, Monika Østensen. (1997) PREGNANCY AND RHEUMATOID ARTHRITIS. Rheumatic Disease Clinics of North America 23:1, 195-212
CrossRef92
B. Aguilar, P.L.A.M. Vos, J.F. Beckers, E.J. Hensen, S.J. Dieleman. (1997) The role of the major histocompatibility complex in bovine embryo transfer. Theriogenology 47:1, 111-120
CrossRef93
Nahoko Asanuma, Akihiro Sakurai, Toru Aizawa, Kiyoshi Hashizume. (1997) Alopecia Universalis With Remission During Pregnancy and Prednisolone Therapy. The American Journal of the Medical Sciences 313:1, 67-69
CrossRef94
BARBARA B. MITTLEMAN, GENE M. SHEARER. (1996) Mother-to-Infant Transmission of HIV Type 1: Role of Major Histocompatibility Antigen Differences. AIDS Research and Human Retroviruses 12:15, 1397-1400
CrossRef95
Dobri D. Kiprov, Robert D. Nachtigall, Roderic C. Weaver, Arnold Jacobson, Elliott K. Main, Marvin R. Garovoy. (1996) The Use of Intravenous Immunoglobulin in Recurrent Pregnancy Loss Associated With Combined Alloimmune and Autoimmune Abnormalities. American Journal of Reproductive Immunology 36:4, 228-234
CrossRef96
Jean-Marie Berthelot, Regis Bataille, Yves Maugars, Alain Prost. (1996) Rheumatoid arthritis as a bone marrow disorder. Seminars in Arthritis and Rheumatism 26:2, 505-514
CrossRef97
Ian C. Chikanza. (1996) The neuroendocrine immunology of rheumatoid arthritis. Baillière's Clinical Rheumatology 10:2, 273-293
CrossRef98
Alan E. Beer, Joanne Y.H. Kwak, Jaime E. Ruiz. (1996) Immunophenotypic Profiles of Peripheral Blood Lymphocytes in Women With Recurrent Pregnancy Losses and in Infertile Women With Multiple Failed In Vitro Fertilization Cycles. American Journal of Reproductive Immunology 35:4, 376-382
CrossRef99
Pierre Miossec, Pascale Chomarat, Julie Dechanet. (1996) Bypassing the antigen to control rheumatoid arthritis. Immunology Today 17:4, 170-173
CrossRef100
J.Y.H. Kwak, F.M.Y. Kwak, S.W. Ainbinder, A.M. Ruiz, A.E. Beer. (1996) Elevated Peripheral Blood Natural Killer Cells Are Effectively Downregulated by Immunoglobulin G Infusion in Women With Recurrent Spontaneous Abortions. American Journal of Reproductive Immunology 35:4, 363-369
CrossRef101
J. Lee Nelson. (1996) Maternal–fetal immunology and autoimmune disease. Is some autoimmune disease auto-alloimmune or allo-autoimmune?. Arthritis & Rheumatism 39:2, 191-194
CrossRef102
Paul Brennan, Tony Payton, Bill Ollier, Alan Silman. (1996) Maternal exposure to paternal HLA does not explain the postpartum increase in rheumatoid arthritis. Genetic Epidemiology 13:4, 411-418
CrossRef103
Alfonse T. Masi, Seth L. Feigenbaum, Robert T. Chatterton. (1995) Hormonal and pregnancy relationships to rheumatoid arthritis: Convergent effects with immunologic and microvascular systems. Seminars in Arthritis and Rheumatism 25:1, 1-27
CrossRef104
Thomas Steck, Katrin van der Ven, Joanne Kwak, Alan Beer, Carole Ober. (1995) HLA-DQA1 and HLA-DQB1 haplotypes in aborted fetuses and couples with recurrent spontaneous abortion. Journal of Reproductive Immunology 29:2, 95-104
CrossRef105
J. C. LORENTZEN, H. ERLANDSSON, A. MUSSENER, L. MATTSSON, S. KLEINAU, U. NYMAN, L. KLARESKOG. (1995) Specific and Long-Lasting Protection from Collagen-Induced Arthritis and Oil-Induced Arthritis in DA Rats by Administration of Immunogens. Scandinavian Journal of Immunology 42:1, 82-89
CrossRef106
Salvatore Albani, Edward C. Keystone, J. Lee Nelson, William E.R. Ollier, Antonio La Cava, Ann C. Montemayor, Deborah A. Weber, Carlomaurizio Montecucco, Alberto Martini, Dennis A. Carson. (1995) Positive selection in autoimmunity: Abnormal immune responses to a bacterial dnaJ antigenic determinant in patients with early rheumatoid arthritis. Nature Medicine 1:5, 448-452
CrossRef107
Reg Hall. (1995) Pregnancy and autoimmune endocrine disease. Baillière's Clinical Endocrinology and Metabolism 9:1, 137-155
CrossRef108
Alan M. Krensky, Carol Clayberger. (1994) Prospects for induction of tolerance in renal transplantation. Pediatric Nephrology 8:6, 772-779
CrossRef109
GERARD N. BURROW. (1994) Thyroid Dysfunction in the Recently Pregnant: Postpartum Thyroiditis. Thyroid 4:3, 363-365
CrossRef110
Oded Abramsky. (1994) Pregnancy and multiple sclerosis. Annals of Neurology 36:S1, S38-S41
CrossRef111
Carole Ober, Thomas Steck, Katrin van der Ven, Christine Billstrand, Lori Messer, Joanne Kwak, Kenneth Beaman, Alan Beer. (1993) MHC class II compatibility in aborted fetuses and term infants of couples with recurrent spontaneous abortion. Journal of Reproductive Immunology 25:3, 195-207
CrossRef112
Gill, Thomas J. III, . (1993) Maternal-Fetal Interactions and Disease. New England Journal of Medicine 329:7, 500-501
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