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白细胞介素-10对粒细胞/巨噬细胞集落刺激因子/白细胞介素-4诱导的HLA II类分子和CD1分子表达的不同影响。

Differential effects of interleukin-10 on the expression of HLA class II and CD1 molecules induced by granulocyte/macrophage colony-stimulating factor/interleukin-4.

作者信息

Thomssen H, Kahan M, Londei M

机构信息

Kennedy Institute of Rheumatology, Sunley Division, Hammersmith, London, GB.

出版信息

Eur J Immunol. 1995 Sep;25(9):2465-70. doi: 10.1002/eji.1830250909.

Abstract

Interleukin (IL)-10 down-regulates HLA class II molecules, whether constitutively expressed or up-regulated by interferon-gamma or IL-4 on monocytes but not on B lymphocytes. In this study we show that IL-10 does not inhibit HLA class II expression induced by the combination granulocyte/macrophage colony-stimulating factor and IL-4 on monocytes, although it simultaneously abrogates the expression of CD1 molecules induced by the same combination of cytokines. CD1 molecules can act as element of genetic restriction for CD4- CD8- T lymphocytes, and the suppression of CD1 expression by IL-10 abolished antigen presentation to CD1-restricted CD4- CD8- T cell receptor-positive T cells. Although HLA class II expression was not down-regulated by IL-10, the antigen specific proliferative response of CD4+ T cells was nevertheless decreased. This was not caused by down-regulation of known co-stimulatory molecules such as B7.1, B7.2 and ICAM-1. IL-10 decreased the antigen specific proliferative response further by directly influencing the T lymphocytes. Our results indicate that IL-10 exerts some of its immunoregulatory functions by differential modulation of antigen presenting molecules, induced by the same combination of cytokines.

摘要

白细胞介素(IL)-10可下调单核细胞上组成性表达的或由干扰素-γ或IL-4上调的HLA-II类分子,但对B淋巴细胞无此作用。在本研究中,我们发现IL-10并不抑制粒细胞/巨噬细胞集落刺激因子与IL-4联合诱导的单核细胞上HLA-II类分子的表达,尽管它同时消除了相同细胞因子组合诱导的CD1分子的表达。CD1分子可作为CD4-CD8-T淋巴细胞遗传限制的元件,IL-10对CD1表达的抑制消除了向CD1限制性CD4-CD8-T细胞受体阳性T细胞的抗原呈递。尽管IL-10未下调HLA-II类分子的表达,但CD4+T细胞的抗原特异性增殖反应仍降低。这不是由已知的共刺激分子如B7.1、B7.2和ICAM-1的下调引起的。IL-10通过直接影响T淋巴细胞进一步降低了抗原特异性增殖反应。我们的结果表明,IL-10通过对相同细胞因子组合诱导的抗原呈递分子的差异调节发挥其一些免疫调节功能。

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