Control of immune pathology by IL-10-secreting regulatory T cells
Control of immune pathology by IL-10-secreting regulatory T cells
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DOI：
10.1007/s002810050068
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发表时间：
1999-12-01
期刊：
影响因子：
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通讯作者：
Powrie, F
中科院分区：
文献类型：
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作者：
Fowler, S;Powrie, F
同样的效应机制，已经进化到保护宿主免受入侵的微生物，如果不适当的调节，可以诱导免疫病理学。许多疾病的致病性是由于诱导了异常的免疫反应。例如，炎症性肠病（IBD）涉及响应于细菌抗原或由细菌抗原驱动的致病性T细胞的激活，而自身免疫性疾病是宿主自身组织激活免疫系统的结果。在遗传易感个体中发生脑型疟疾归因于寄生虫诱导的TNF产生[15]，表明对感染因子的过度或失调的免疫应答也可诱发疾病。尽管免疫系统有能力杀死宿主，但炎症性疾病并不常见，这表明存在限制免疫反应的机制，并且在某些情况下，完全抑制免疫反应。现在有越来越多的证据表明，功能特化的调节性T细胞（Treg）群体在这一过程中发挥主导作用。具有Treg特征的T细胞已在许多模型系统中描述[25]。本文就分泌免疫抑制细胞因子IL-10和转化生长因子-[3]（TGF-Ⅰ）的细胞作一综述。
The same effector mechanisms that have evolved to protect the host from invading micro-organisms can, if inappropriately regulated, induce immune pathology. A number of diseases owe their pathogenicity to the induction of aberrant immune responses. For example, inflammatory bowel disease (IBD) involves the activation of pathogenic T cells responding to or driven by bacterial antigens, and autoimmune disease is a consequence of the activation of the immune system by the hosts own tissues. The development of cerebral malaria in genetically susceptible individuals is attributed to parasite-induced TNF production [15], indicating that an over zealous or dysregulated immune response to an infectious agent can also induce disease. Despite the ability of the immune system to kill the host, inflammatory diseases are infrequent, suggesting that there are mechanisms that limit the immune response and, in some instances, suppress it completely. There is now accumulating evidence that functionally specialised populations of regulatory T cells (Treg) play a dominant role in this process. T cells with the characteristics of Treg have been described in a number of model systems [25]. In this review we focus on those cells secreting the immunosuppressive cytokines IL-10 and transforming growth factor-[3 (TGF-I]).