کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5666758 | 1591546 | 2016 | 7 صفحه PDF | دانلود رایگان |
- ZnT8107-115/HLA-A2 dimers inhibited proliferation, cytotoxicity, and inflammatory cytokine of CD8+ T.
- ZnT8107-115/HLA-A2 dimers ameliorated the incidence and severity of diabetes mice.
- ZnT8107-115/HLA-A2 dimers abrogate pathogenic CD8+ T cells in diabetes.
Recent studies demonstrated that activated CD8+ T cells contributed to the development of T1D, and Zinc Transporter 8 (ZnT8) has emerged as a target of autoreactive T cells in human T1D in recent years. In the previous work, we identified that ZnT8107-115 peptide as a candidate to generate CD8+ T cells and induce diabetes in mice. In addition, MHC-peptide complexes that interact with autoreactive T cells can induce immune tolerance. In the current study, we constructed ZnT8107-115/HLA-A2 dimers, and utilized them to immunize diabetes mice. The proliferation, cytotoxicity, and inflammatory cytokine of CD8+ T were analyzed, and the incidence and severity of diabetes were detected.We found that ZnT8107-115/HLA-A2 dimers inhibited proliferation, cytotoxicity, and inflammatory cytokine of CD8+ T. Additionally, ZnT8107-115/HLA-A2 dimers ameliorated the incidence and severity of diabetes mice. Our findings suggested that ZnT8107-115/HLA-A2 dimers abrogate pathogenic CD8+ T cells in diabetes, and the strategies represented promising way in T1D and other autoimmune diseases.
Journal: Immunology Letters - Volume 180, December 2016, Pages 66-72