Lesional activation of T c 17 cells in Behçet disease and psoriasis supports HLA class I‐mediated autoimmune responses*
| العنوان: | Lesional activation of T c 17 cells in Behçet disease and psoriasis supports HLA class I‐mediated autoimmune responses* |
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| المؤلفون: | Daniela Hartmann, Yukiyasu Arakawa, Aylin Okçu Heper, Sigrid Vollmer, K. Kerl, Ayşe Boyvat, A. Karal-Öktem, A. Arakawa, Jörg C. Prinz, P. Ertop Doğan, U. Puchta, M. He, Seçil Vural |
| المساهمون: | Vural, Seçil (ORCID 0000-0001-6561-196X & YÖK ID 189340), Kerl, K., Doğan, P. Ertop, Vollmer, S., Puchta, U., He, M., Arakawa, Y., Heper, A. O., Karal Öktem, A, Hartmann, D., Boyvat, A., Prinz, J. C., Arakawa, A., School of Medicine |
| المصدر: | British Journal of Dermatology |
| بيانات النشر: | Oxford University Press (OUP), 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | Behcet Syndrome, Uveitis, Infliximab, Autoimmune disease, CD68, business.industry, CD11c, Dermatology, Neutrophil extracellular traps, Human leukocyte antigen, medicine.disease, Antigen, Psoriasis, Immunology, medicine, business, CD8 |
| الوصف: | Background: Behcet 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: we found that in BD lesions, as in psoriasis, actively expanding CD8(+) T cells were the predominant source of IL-17A. IL-17A(+) CD8(+) T (T(c)17) cells outnumbered infiltrating IL-17A(+) CD4(+) T cells. Unlike the epidermal localization of CD8(+) T cells in psoriasis, T(c)17 cells in BD lesions mainly infiltrated the perivascular tissue and the blood vessel walls of dermis and subcutaneous tissue. They co-localised with a marked IL-23A expression by CD11c(+) dendritic cells and CD68(+) macrophages. IL-17A expression was associated with extensive recruitment of neutrophils around blood vessels that formed neutrophil extracellular traps (NETs). Conclusions: in BD, the genetic predisposition may mediate antigen-specific activation and differentiation of a T(c)17 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. Deutsche Forschungsgemeinschaft; Scientific and Technological Research Council of Turkey (TÜBİTAK); 2219 Postdoctoral Research Grant; L'OREAL-UNESCO for Women in Science Fellowship of Turkey; LMU–China Scholarship Council Program Full Doctoral Study-Model; Projekt DEAL |
| وصف الملف: | text/academic publication |
| تدمد: | 1365-2133 0007-0963 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::29c342d264af4f0b9f8e373140d61f83 https://doi.org/10.1111/bjd.20643 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....29c342d264af4f0b9f8e373140d61f83 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 13652133 00070963 |
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