Lesional activation of T(c)17 cells in Behcet disease and psoriasis supports HLA class I-mediated autoimmune responses

Vural, S.; Kerl, K.; Dogan, P.; Vollmer, S.; Puchta, U.; He, M.; Arakawa, Y.; Heper, AYLİN; Karal-Oktem, AYŞE; Hartmann, D.; Boyvat, AYŞE; Prinz, J.; Arakawa, A.

doi:10.1111/bjd.20643

Lesional activation of T(c)17 cells in Behcet disease and psoriasis supports HLA class I-mediated autoimmune responses

Atıf İçin Kopyala

Vural S., Kerl K., Dogan P. E., Vollmer S., Puchta U., He M., ...Daha Fazla

BRITISH JOURNAL OF DERMATOLOGY, cilt.185, sa.6, ss.1209-1220, 2021 (SCI-Expanded)

Yayın Türü: Makale / Tam Makale
Cilt numarası: 185 Sayı: 6
Basım Tarihi: 2021
Doi Numarası: 10.1111/bjd.20643
Dergi Adı: BRITISH JOURNAL OF DERMATOLOGY
Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, BIOSIS, CAB Abstracts, EMBASE, International Pharmaceutical Abstracts, MEDLINE, Veterinary Science Database
Sayfa Sayıları: ss.1209-1220
Ankara Üniversitesi Adresli: Evet

Özet

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.