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干扰素诱导的 HIN-200 基因家族在细胞凋亡和炎症中的作用:与自身免疫的关系。

The interferon-inducible HIN-200 gene family in apoptosis and inflammation: implication for autoimmunity.

机构信息

NoToPharm srl, Colleretto Giacosa (TO), Turin, Italy.

出版信息

Autoimmunity. 2010 Apr;43(3):226-31. doi: 10.3109/08916930903510922.

Abstract

The Ifi-200/HIN-200 gene family encodes highly homologous human (IFI16, myeloid cell nuclear differentiation antigen, absent in melanoma 2, and IFIX) and murine proteins (Ifi202a, Ifi202b, Ifi203, Ifi204, Ifi205, and Ifi206), which are induced by type I and II interferons (IFN). These proteins have been described as regulators of cell proliferation and differentiation and, more recently, several reports have suggested their involvement in both apoptotic and inflammatory processes. The relevance of HIN-200 proteins in human disease is beginning to be clarified, and emerging experimental data indicate their role in autoimmunity. Autoimmune disorders are sustained by perpetual activation of inflammatory process and a link between autoimmunity and apoptosis has been clearly established. Moreover, the interferon system is now considered as a key player in autoimmune disorders such as systemic lupus erythemathosus, systemic sclerosis, and Sjögren's syndrome, and it is therefore conceivable to hypothesize that HIN-200 may be among the pivotal mediators of IFN activity in autoimmune disease. In particular, the participation of HIN-200 proteins in apoptosis and inflammation could support their potential role in autoimmunity.

摘要

IFI16、髓系细胞核分化抗原、黑色素瘤 2 缺失因子和 IFIX)和鼠源蛋白(Ifi202a、Ifi202b、Ifi203、Ifi204、Ifi205 和 Ifi206),这些蛋白由 I 型和 II 型干扰素(IFN)诱导。这些蛋白已被描述为细胞增殖和分化的调节剂,最近的几份报告表明它们参与了细胞凋亡和炎症过程。HIN-200 蛋白在人类疾病中的相关性开始被阐明,新兴的实验数据表明它们在自身免疫中的作用。自身免疫性疾病是由炎症过程的持续激活维持的,并且自身免疫与细胞凋亡之间的联系已经得到明确证实。此外,干扰素系统现在被认为是系统性红斑狼疮、系统性硬皮病和干燥综合征等自身免疫性疾病的关键参与者,因此可以假设 HIN-200 可能是自身免疫疾病中 IFN 活性的关键介质之一。特别是,HIN-200 蛋白在细胞凋亡和炎症中的参与可能支持它们在自身免疫中的潜在作用。

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