Correspondence

Allergy and IgE Antibodies

N Engl J Med 2001; 344:1332-1333April 26, 2001

Article

To the Editor:

Allergic symptoms are the result of an inflammatory process triggered by an allergen or allergens to which a patient has generated antibodies after a previous exposure. Dr. Kay's review article on allergic diseases (Jan. 4 issue)1 recognizes only the action of IgE in the inflammatory process and erroneously identifies a response mediated by type 2 helper T cells (Th2) as an exclusively IgE response, ignoring the other epitopes. This may be the result of using immediate hypersensitivity skin-prick tests as the sole means to detect the patient's allergic reactivities. Such tests detect only IgE antibodies. I believe the article is seriously flawed because it ignores the most efficient inflammatory antibodies generated on exposure to antigen — namely, IgG and IgM.

Vincent A. Marinkovich, M.D.
801 Brewster Ave., Redwood City, CA 94063

1 References

1. 1

   Kay AB. Allergy and allergic diseases. N Engl J Med 2001;344:30-37
   Full Text | Web of Science | Medline

Author/Editor Response

Dr. Kay replies:

To the Editor: Although Dr. Marinkovich is correct to point out that Th2 cells direct the synthesis of IgG, not just of IgE, there is little evidence that antibodies other than IgE cause appreciable damage to tissue in atopic allergic disease. In fact, several studies suggest that IgG, produced either by natural exposure1 or during immunotherapy2 (and often referred to as “blocking antibodies”), may be protective. Furthermore, both persons with atopy and those without atopy produce house-dust-mite–specific and grass-pollen–specific IgG1 and IgG4.3 On the other hand, there are several nonatopic hypersensitivity disorders (which are usually outside the province of the allergist) in which IgG antibodies are clearly pathogenic.

In Gell and Coombs type II (cytolytic or cytotoxic) hypersensitivity reactions, IgG antibodies facilitate the destruction of cells by interacting with antigen on cell surfaces; such damage is the cause of autoimmune hemolytic anemia and certain types of transfusion reactions. IgG can also stimulate cells and so alter their function (or signaling) either as an agonist (e.g., in the case of thyrotropin in Graves' disease) or antagonist (e.g., in the case of anti–acetylcholine-receptor antibody in myasthenia gravis). In type III hypersensitivity reactions (or Arthus-type reactions), antigen–antibody complexes in and around the microvasculature activate complement, leading to a neutrophil-rich inflammatory response and subsequent tissue injury. Examples include immune-complex glomerulonephritis, classic serum sickness, and the farmer's lung group of diseases (hypersensitivity pneumonitis). The role of IgE, IgG, type 1 helper T cells, and Th2 cells in the pathogenesis of the hypersensitivity disorders is discussed in more detail elsewhere.4

A.B. Kay, M.D., Ph.D.
National Heart and Lung Institute, London SW3 6LY, United Kingdom

4 References

1. 1

   Golden DB, Meyers DA, Kagey-Sobotka A, Valentine MD, Lichtenstein LM. Clinical relevance of the venom-specific immunoglobulin G antibody level during immunotherapy. J Allergy Clin Immunol 1982;69:489-493
   CrossRef | Web of Science | Medline

2. 2

   Witteman AM, Stapel SO, Sjamsoedin DH, Jansen HM, Aalberse RC, van der Zee JS. Fel d 1-specific IgG antibodies induced by natural exposure have blocking activity in skin tests. Int Arch Allergy Immunol 1996;109:369-375
   CrossRef | Web of Science | Medline

3. 3

   Kemeny DM, Urbanek R, Ewan P, et al. The subclass of IgG antibody in allergic disease. II. The IgG subclass of antibodies produced following natural exposure to dust mite and grass pollen in atopic and nonatopic individuals. Clin Exp Allergy 1989;19:545-549
   CrossRef | Web of Science | Medline

4. 4

   Kay AB. Concepts of allergy and hypersensitivity. In: Kay AB, ed. Allergy and allergic diseases. Vol. 1. Oxford, England: Blackwell Science, 1997:23-35.
   

Citing Articles (1)

Citing Articles

1. 1

   Yousri M. Hussein, Shereen A. El-Tarhouny, Sally M. Shalaby, Randa H. Mohamed, Tamer H. Hassan, Hend M. El-Sherbeny, Noha A. Mohamed. (2011) Interleukin-13 Receptor A1 Gene Polymorphism and IL-13 Serum Level in Atopic and Non-atopic Egyptian Children. Immunological Investigations1-12
   CrossRef