| Summary: | Elias Toubi,1 Zahava Vadasz2 1The Outpatient Allergy Clinic, The Holy Family Hospital, Nazareth, Israel; 2The Proteomic Unit, The Division of Clinical Immunology, Bnai-Zion Medical Center, Faculty of Medicine, Technion, Haifa, IsraelCorrespondence: Zahava Vadasz Email zahava.vadas@b-zion.org.ilAbstract: 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.Keywords: IL-17, interleukin-17, chronic spontaneous urticaria, CSU, T cells, mast cells
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