Linking allergy to autoimmune disease.
Type I allergy is a classical Th2-driven hypersensitivity disease based on IgE recognition of environmental allergens. Exposure of allergic individuals to exogenous allergens leads to immediate type inflammation caused by degranulation of mast cells via IgE-allergen immune complexes and the release of inflammatory mediators, proteases and pro-inflammatory cytokines. However, allergic inflammation can occur and persist in the absence of exposure to exogenous allergens and might paradoxically resemble a Th1-mediated chronic inflammatory reaction. We summarize evidence supporting the view that autoimmune mechanisms might contribute to these processes. IgE recognition of autoantigens might augment allergic inflammation in the absence of exogenous allergen exposure. Moreover, autoantigens that activate Th1-immune responses could contribute to chronic inflammation in allergy, thus linking allergy to autoimmunity.
Valenta
Rudolf
R
Division of Immunopathology, Department of Pathophysiology, Center for Physiology and Pathophysiology, Medical University of Vienna, A-1090 Vienna, Austria. rudolf.valenta@meduniwien.ac.at
Mittermann
Irene
I
Werfel
Thomas
T
Garn
Holger
H
Renz
Harald
H
D000485:Allergens / Q000276:immunology; D000818:Animals; D001323:Autoantibodies / Q000097:blood*; D001324:Autoantigens / Q000276:immunology* / Q000378:metabolism; D015551:Autoimmunity / Q000276:immunology*; D003429:Cross Reactions / Q000276:immunology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology* / Q000378:metabolism; D007073:Immunoglobulin E / Q000097:blood*; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism
D000485:Allergens; D001323:Autoantibodies; D001324:Autoantigens; D016207:Cytokines; D007073:Immunoglobulin E