Anti-IgE autoantibodies: a possible specific feedback on the cytokine network in allergy?
We propose a theoretical model based on the cytokine network, that provides the necessary signals so that basically all human beings can produce IgE but not all have to develop allergic disease. Our hypothesis implies that anti-IgE autoantibodies are a kind of emergency brake neutralizing the IgE induced by the cytokine network. In the normal individual the system would come to halt at this point. However, the atopic individual, due to a small difference in his or her B cell repertoire, will produce the wrong type of anti-IgE antibody. Allergic disease can now develop because IgE is not perfectly neutralized. The wrong type of anti-IgE antibody that is now produced may even aggravate the disease as some of these autoantibodies may induce IgE synthesis or trigger effector cells that in turn generate a Th2 like cytokine pattern closing the vicious circle. We believe that because of the potency of the powerful and archaic cytokine network, we have to dispose of such a specific control mechanism by autoantibodies.
Stadler
B M
BM
Institute of Clinical Immunology, University of Bern, Inselspital, Switzerland.
D000888:Antibodies, Anti-Idiotypic / Q000276:immunology*; D001323:Autoantibodies / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D016207:Cytokines / Q000502:physiology*; D005246:Feedback; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D007073:Immunoglobulin E / Q000276:immunology*; D008954:Models, Biological; D013601:T-Lymphocytes / Q000276:immunology
D000888:Antibodies, Anti-Idiotypic; D001323:Autoantibodies; D016207:Cytokines; D007073:Immunoglobulin E