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A&R:抗双链 DNA 抗体可识别系统性红斑狼疮风险等位基因的 HLA II 类分子上呈递的 DNA

2022-01-23 MedSci原创 MedSci原创

DNA以类似于错误折叠蛋白质的方式与HLA II类分子结合,并且与HLA II类分子结合的DNA通过激活表达抗DNA的B细胞受体方式激活B细胞,从而参与 SLE发病机制。

      目的:特定的HLA II类等位基因与系统性红斑狼疮(SLE)的易感性相关。HLA II 类分子在SLE发病机制中的作用仍不清楚,尽管抗DNA抗体对SLE具有特异性并且与疾病活动相关。研究人员之前证明,与HLA II类分子结合的错误折叠蛋白是自身免疫性疾病中产生的自身抗体的特异性靶标。本研究旨在验证以下假设:DNA以类似于错误折叠蛋白质的方式与HLA II类分子结合,并且与HLA II类分子结合的DNA通过激活表达抗DNAB细胞受体方式激活B细胞,从而参与 SLE发病机制。

     方法:研究团队对SLE患者进行HLA基因分型,在B16-F10细胞中采用CRISPR-Cas9敲除MHCII从而用于分析DNAHLA II 类分子的结合,以及表达抗DNA B细胞受体(BCR)的细胞对表达DNA/HLA II类复合物的细胞的反应。

    结果:SLE的风险等位基因中观察到DNAHLA II类分子的有效结合,例如 HLA-DRB1*15:01DNA与每个HLA-DR等位基因结合的效率与HLA-DR等位基因赋予的SLE风险呈正相关。此外,携带抗DNA BCR的报告细胞被表达DNA/HLA II类复合物的细胞激活。研究证明了细胞表面的DNA 表达通过与 MHC II 类分子结合而发生。DNAHLA-DR等位基因结合的效率显著与每个人HLA-DR等位基因所赋予的SLE风险的优势比相关。这表明具有HLA-DR等位基因可能与DNA形成复合物的的个体比不具有与DNA形成复合物的HLA-DR等位基因的个体更容易发展成SLE

    结论:这些结果提供了与 HLA II类分子结合的DNA参与 SLE 发病机制的证据。

 

出处:

Tsuji, H., Ohmura, K., Jin, H., Naito, R., Arase, N., Kohyama, M., Suenaga, T., Sakakibara, S., Kochi, Y., Okada, Y., Yamamoto, K., Kikutani, H., Morinobu, A., Mimori, T. and Arase, H. (2022), Anti–Double-Stranded DNA Antibodies Recognize DNA Presented on HLA Class II Molecules of Systemic Lupus Erythematosus Risk Alleles. Arthritis Rheumatol, 74: 105-111. https://doi.org/10.1002/art.41897

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    2022-01-24 zhouqu_8
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    2022-01-24 marongnuan

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