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哮喘、过敏和自身免疫中的 T 细胞免疫球蛋白和黏蛋白结构域(Tim)基因家族。

The T-cell immunoglobulin and mucin domain (Tim) gene family in asthma, allergy, and autoimmunity.

机构信息

Department of Medicine, Nassau University Medical Center, East Meadow, NY 11554, USA.

出版信息

Allergy Asthma Proc. 2013 Jan-Feb;34(1):e21-6. doi: 10.2500/aap.2013.34.3646.

Abstract

The T-cell immunoglobulin and mucin domain (Tim) gene family is a relatively newly discovered group of molecules with a conserved structure and important immunologic functions. Tim molecules express on many types of immune cells including T cells, B cells, dendritic cells, macrophages, and mast cells that have been shown to be involved in asthma, allergic rhinitis, food allergy, and autoimmunity. Tim-1-Tim-4 interaction promotes Th2 cytokine responses, and blocking this interaction can decrease airway inflammation in asthma and in allergic rhinitis. Tim-3 stimulates mast cells to produce Th2 cytokines, and anti-Tim-3 is able to dampen asthmatic inflammation. The Tim-3 ligand was shown to be greatly enhanced on intestinal epithelial cells in patients with food allergy and Tim-4 may play a role in maintaining oral tolerance and prevention of food allergy. Tim-3 deregulation plays a role in the pathogenesis of multiple sclerosis. Increased Tim-1 expression has been shown in mononuclear cells from systemic lupus erythematosus patients and Tim-3 may be involved in a protective role in rheumatoid arthritis.

摘要

T 细胞免疫球蛋白和黏蛋白结构域(Tim)基因家族是一组相对较新发现的分子,具有保守的结构和重要的免疫功能。Tim 分子在许多类型的免疫细胞上表达,包括 T 细胞、B 细胞、树突状细胞、巨噬细胞和肥大细胞,这些细胞已被证明与哮喘、过敏性鼻炎、食物过敏和自身免疫有关。Tim-1-Tim-4 相互作用促进 Th2 细胞因子反应,阻断这种相互作用可以减少哮喘和过敏性鼻炎中的气道炎症。Tim-3 刺激肥大细胞产生 Th2 细胞因子,抗 Tim-3 能够抑制哮喘炎症。研究表明,食物过敏患者的肠道上皮细胞上 Tim-3 配体大大增强,而 Tim-4 可能在维持口服耐受和预防食物过敏方面发挥作用。Tim-3 失调在多发性硬化症的发病机制中起作用。系统性红斑狼疮患者的单核细胞中显示出增加的 Tim-1 表达,而 Tim-3 可能在类风湿关节炎中发挥保护作用。

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