Open AccessThe Emerging Role of IL-17 in the Immune-Pathogenesis of Chronic Spontaneous Urticaria
Author(s) -
Elias Toubi,
Zahava Vadasz
Publication year - 2020
Publication title -
immunotargets and therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.256
H-Index - 7
ISSN - 2253-1556
DOI - 10.2147/itt.s266410
Subject(s) - immunology , omalizumab , pathogenesis , medicine , degranulation , immune system , immunoglobulin e , antigen , mast cell , disease , histamine , interleukin 33 , autoantibody , secukinumab , interleukin , psoriasis , antibody , cytokine , receptor , pathology , psoriatic arthritis
Chronic spontaneous urticaria (CSU) is considered to be an autoimmune disorder (type I and type II) in 50% of all cases. However, autoreactive T cells and their proximity with activated mast cells in the skin of CSU patients are believed to be the primary event in mast cell degranulation. The finding of anti-FcɛRIα on mast cells or IgE autoantibodies against thyroid antigens should be considered to be a consequence of the auto-reactive T cells' recognition of the above-mentioned antigens. Our recent finding of increased Th17 and IL-17 expression in both CD4+ T cells and mast cells in the skin of severe CSU patients is supportive for the major role that T cells perform in the pathogenesis of CSU. Supporting this are numerous previous reports in which increased serum IL-17 was found to be in association with CSU disease severity. The beneficial effect of anti-IL-17A (secukinumab) in CSU patients in whom high dose anti-histamines, recurrent course of steroids and omalizumab fail to achieve a reasonable response should be investigated as a new therapeutic strategy in future studies with a large cohort of patients.