
We aimed to determine pathological changes in Behçet disease (BD) skin lesions related to the complex genetic predisposition. In BD, the genetic predisposition may mediate antigen‐specific activation and differentiation of a Tc17 response, possibly targeting endothelial (auto)antigens. Neutrophils recruited by IL‐17A in this process may enhance tissue damage by extensive NET formation (NETosis). Thus, the IL‐23/IL‐17 axis presumably controls neutrophilic inflammation in BD vasculitis in the context of a predominant antigen‐specific CD8+ T‐cell response.
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