دورية أكاديمية
HLA‐DR3介导的CD4 T细胞对1型糖尿病患者GAD65的应答
| العنوان: | HLA‐DR3介导的CD4 T细胞对1型糖尿病患者GAD65的应答 |
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| المؤلفون: | Neihenuo Chuzho, Neetu Mishra, Nikhil Tandon, Uma Kanga, Gunja Mishra, Akanksha Sharma, Narinder K. Mehra, Neeraj Kumar |
| المصدر: | Journal of Diabetes, Vol 15, Iss 7, Pp 607-621 (2023) |
| بيانات النشر: | Wiley, 2023. |
| سنة النشر: | 2023 |
| المجموعة: | LCC:Diseases of the endocrine glands. Clinical endocrinology |
| مصطلحات موضوعية: | CD4 T细胞, 细胞因子, GAD65, HLA, 1型糖尿病, Diseases of the endocrine glands. Clinical endocrinology, RC648-665 |
| الوصف: | Abstract Aim We planned this study to identify diabetogenic glutamic acid decarboxylase (GAD65) peptides possibly responsible for human leucocyte antigen (HLA)‐DR3/DQ2‐mediated activation of GAD65‐specific CD4 T cells in type 1 diabetes (T1D). Methods Top 30 GAD65 peptides, found to strongly bind in silico with HLA‐DR3/DQ2 molecules, were selected and grouped into four pools. The peptides were used to stimulate CD4 T cells of study subjects in 16‐h peripheral blood mononuclear cell culture. CD4 T cells' stimulation in terms of interferon‐gamma (IFN‐γ), interleukin (IL)‐17, tumor necrosis factor‐alpha (TNF‐α), and IL‐10 expression was analyzed using flow cytometry. Results Although all four GAD65 peptide pools (PP1‐4) resulted in significantly higher expression of IFN‐γ by CD4 T cells (p = .003, p |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1753-0407 1753-0393 |
| العلاقة: | https://doaj.org/toc/1753-0393Test; https://doaj.org/toc/1753-0407Test |
| DOI: | 10.1111/1753-0407.13406 |
| الوصول الحر: | https://doaj.org/article/29ef37f916e442c4abfe137d2e417e0cTest |
| رقم الانضمام: | edsdoj.29ef37f916e442c4abfe137d2e417e0c |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 17530407 17530393 |
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| DOI: | 10.1111/1753-0407.13406 |