四跨膜蛋白 CD53：一种被忽视的免疫细胞功能调节因子。,Medical Microbiology and Immunology

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四跨膜蛋白 CD53：一种被忽视的免疫细胞功能调节因子。
Medical Microbiology and Immunology ( IF 5.5 ) Pub Date : 2020-05-21 , DOI: 10.1007/s00430-020-00677-z
V E Dunlock ₁

Affiliation

四跨膜蛋白是膜组织蛋白，通过形成由四跨膜蛋白及其伴侣蛋白组成的亚细胞结构域，在组织细胞表面方面发挥作用。这些复合物被称为富含四跨膜蛋白的微域（TEM）或四跨膜蛋白网。TEM 的形成可以调节多种细胞过程，例如粘附、迁移、信号传导和细胞融合。四跨膜蛋白 CD53 是四跨膜蛋白超家族的成员，仅在免疫区室中表达。其中，B 细胞、CD4 ⁺ T 细胞、CD8 ⁺ T 细胞、树突状细胞、巨噬细胞和自然杀伤细胞都被发现在其表面表达高水平的这种蛋白质。大约三十年前，有报道称缺乏 CD53 的患者对病原体的易感性增加，导致反复出现病毒、细菌和真菌感染的临床表现。这清楚地表明 CD53 在免疫功能中具有重要且非冗余的作用。然而，尽管有这一惊人的发现，CD53 在免疫系统中的具体功能作用仍然难以捉摸。本综述旨在对已发表的有关 CD53 的文献进行简明概述，并反思该蛋白在免疫细胞调节和功能中未被充分认识的作用。

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Tetraspanin CD53: an overlooked regulator of immune cell function.

Tetraspanins are membrane organizing proteins that play a role in organizing the cell surface through the formation of subcellular domains consisting of tetraspanins and their partner proteins. These complexes are referred to as tetraspanin enriched microdomains (TEMs) or the tetraspanin web. The formation of TEMs allows for the regulation of a variety of cellular processes such as adhesion, migration, signaling, and cell fusion. Tetraspanin CD53 is a member of the tetraspanin superfamily expressed exclusively within the immune compartment. Amongst others, B cells, CD4⁺ T cells, CD8⁺ T cells, dendritic cells, macrophages, and natural killer cells have all been found to express high levels of this protein on their surface. Almost three decades ago it was reported that patients who lacked CD53 suffered from an increased susceptibility to pathogens resulting in the clinical manifestation of recurrent viral, bacterial, and fungal infections. This clearly suggests a vital and non-redundant role for CD53 in immune function. Yet, despite this striking finding, the specific functional roles of CD53 within the immune system have remained elusive. This review aims to provide a concise overview of the published literature concerning CD53 and reflect on the underappreciated role of this protein in immune cell regulation and function.

更新日期：2020-05-21

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