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Galectin-9 regulates T helper cell function independently of Tim-3

机译:Galectin-9独立于Tim-3调节T辅助细胞功能

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摘要

β-Galactoside-binding lectin 9 (galectin-9) is a tandem repeat-type member of the galectin family. It was initially characterized as an eosinophil chemoattractant and an inducer of apoptosis in thymocytes. Subsequently, galectin-9 was identified as a ligand for transmembrane immunoglobulin mucin domain 3 (Tim-3), a type I glycoprotein induced on T cells during chronic inflammation. Work in autoimmune diseases and chronic viral infections have led to the current hypothesis that the function of Tim-3 is to limit immune responses. However, it is still not known to what degree these effects are due to the galectin-9/Tim-3 interaction. In this study, we show that galectin-9 is not limited to the role of a pro-apoptotic agent, but that it can also induce the production of pro-inflammatory cytokines from T helper cells. This effect is dose-dependent and does not require Tim-3. These findings suggest that the effects of galectin-9 on T cells are more complex than previously thought and are mediated by additional receptors apart from Tim-3.
机译:β-半乳糖苷结合凝集素9(半乳凝素-9)是半乳凝素家族的串联重复型成员。最初被表征为嗜酸性粒细胞趋化剂和胸腺细胞凋亡的诱导剂。随后,半乳凝素9被确定为跨膜免疫球蛋白粘蛋白域3(Tim-3)的配体,该蛋白是在慢性炎症期间在T细胞上诱导的I型糖蛋白。在自身免疫性疾病和慢性病毒感染方面的工作已导致当前的假说,即Tim-3的功能是限制免疫反应。但是,尚不清楚这些作用在何种程度上是由于半乳凝素9 / Tim-3相互作用引起的。在这项研究中,我们表明半乳凝素9不仅限于促凋亡剂的作用,而且还可以诱导T辅助细胞产生促炎性细胞因子。此作用是剂量依赖性的,不需要Tim-3。这些发现表明,galectin-9对T细胞的作用比以前认为的更为复杂,并且由Tim-3以外的其他受体介导。

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