Lesional activation of T <sub>c</sub> 17 cells in Behçet disease and psoriasis supports HLA class I‐mediated autoimmune responses*
Seçil Vural, Katrin Kerl, Pelin Ertop Doğan, Sigrid Vollmer, Ursula Puchta, M. L. He, Yukiyasu Arakawa, Aylın Okçu Heper, A. Karal‐Öktem, Daniela Hartmann, Ayşe Boyvat, Jörg C. Prinz, Akiko Arakawa
Abstract
BACKGROUND: Behçet disease (BD) presents with lymphocytic and neutrophilic vasculitis of unknown aetiology. HLA-B*51, the endoplasmic reticulum aminopeptidase 1 (ERAP1), and interleukin 23 receptor (IL23R)/IL12R are genetic risk factors. IL-23 regulates IL-17A, which controls the recruitment and activation of neutrophils. OBJECTIVES: To determine pathological changes in BD skin lesions related to the complex genetic predisposition. METHODS: We characterized the expression of IL-17A and IL-23A in various cell types by immunohistological double staining of sections from papulopustular skin lesions of acute attacks of BD and psoriasis vulgaris lesions, another HLA-class I-associated T-cell-mediated autoimmune disease in which excessive T-cell-derived IL-17A production promotes neutrophil activation. RESULTS: macrophages. IL-17A expression was associated with extensive recruitment of neutrophils around blood vessels that formed neutrophil extracellular traps (NETs). CONCLUSIONS: T-cell response.