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引用次数: 0
摘要
TNIP1 是之前发现的一种自身免疫风险因子，它能调节线粒体自噬体的转运。TNIP1 的错义突变会破坏这种调节功能，导致 B 细胞内在易感性，诱发以 IgG4 自身抗体和年龄相关 B 细胞扩增为特征的 TLR7 介导的自身免疫病。
TNIP1, a previously identified risk factor for autoimmunity, regulates mitochondrial autophagosomal trafficking. Missense mutations in TNIP1 disrupt this regulatory function, yielding a B cell-intrinsic predisposition for TLR7-mediated autoimmunity characterized by IgG4 autoantibodies and the expansion of age-associated B cells.
期刊介绍：
Nature Immunology is a monthly journal that publishes the highest quality research in all areas of immunology. The editorial decisions are made by a team of full-time professional editors. The journal prioritizes work that provides translational and/or fundamental insight into the workings of the immune system. It covers a wide range of topics including innate immunity and inflammation, development, immune receptors, signaling and apoptosis, antigen presentation, gene regulation and recombination, cellular and systemic immunity, vaccines, immune tolerance, autoimmunity, tumor immunology, and microbial immunopathology. In addition to publishing significant original research, Nature Immunology also includes comments, News and Views, research highlights, matters arising from readers, and reviews of the literature. The journal serves as a major conduit of top-quality information for the immunology community.
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