Sialic acids and autoimmune disease.
Sialic acids and autoimmune disease.
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DOI：
10.1111/imr.12344
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发表时间：
2016-01
影响因子：
8.7
通讯作者：
Pillai S
中科院分区：
文献类型：
--
作者：
Mahajan VS;Pillai S
导致自身免疫的一个重要的潜在机制是免疫系统中抑制性信号的丢失。唾液酸识别IG超家族凝集素或Siglecs是在造血细胞中大量表达的细胞表面蛋白家族。大多数Siglecs是在免疫细胞中表达的抑制性受体，其结合含唾液酸的配体并将含SH 2结构域的酪氨酸磷酸酶募集到其细胞质尾。它们传递抑制信号，可以有助于约束免疫细胞，从而保护宿主免受自身免疫。本文详细介绍了CD 22/Siglec-2和Siglec-G的抑制功能及其对免疫耐受和自身免疫的作用，主要是在B淋巴细胞背景下。相关的自身免疫和炎症的修饰唾液酸，修饰唾液酸的酶，和其他唾液酸结合蛋白也进行了审查。
An important underlying mechanism that contributes to autoimmunity is the loss of inhibitory signaling in the immune system. Sialic acid-recognizing Ig superfamily lectins or Siglecs are a family of cell surface proteins largely expressed in hematopoietic cells. The majority of Siglecs are inhibitory receptors expressed in immune cells that bind to sialic acid containing ligands and recruit SH2-domain containing tyrosine phosphatases to their cytoplasmic tails. They deliver inhibitory signals that can contribute to the constraining of immune cells and thus protect the host from autoimmunity. The inhibitory functions of CD22/Siglec-2 and Siglec-G and their contributions to tolerance and autoimmunity, primarily in the B lymphocyte context, are considered in some detail in this review. The relevance to autoimmunity and unregulated inflammation of modified sialic acids, enzymes that modify sialic acid, and other sialic acid binding proteins are also reviewed.