Department of Dermatology, Brigham and Women's Hospital, Boston, MA 02115, USA.
J Immunol. 2012 Apr 1;188(7):3127-37. doi: 10.4049/jimmunol.1103433. Epub 2012 Feb 17.
Galectin-1 (Gal-1), a β-galactoside-binding protein, can alter fate and effector function of Th cells; however, little is known about how Gal-1 induces Th cell differentiation. In this article, we show that both uncommitted and polarized Th cells bound by Gal-1 expressed an immunoregulatory signature defined by IL-10. IL-10 synthesis was stimulated by direct Gal-1 engagement to cell surface glycoproteins, principally CD45, on activated Th cells and enhanced by IL-21 expression through the c-Maf/aryl hydrocarbon receptor pathway, independent of APCs. Gal-1-induced IL-10(+) T cells efficiently suppressed T cell proliferation and T cell-mediated inflammation and promoted the establishment of cancer immune-privileged sites. Collectively, these findings show how Gal-1 functions as a major glycome determinant regulating Th cell development, inflammation, and tumor immunity.
半乳糖凝集素-1（Gal-1）是一种β-半乳糖苷结合蛋白，可改变 Th 细胞的命运和效应功能；然而，关于 Gal-1 如何诱导 Th 细胞分化知之甚少。在本文中，我们表明，与 Gal-1 结合的未定向和极化 Th 细胞均表达了由 IL-10 定义的免疫调节特征。IL-10 的合成受到刺激，这是通过 Gal-1 与激活的 Th 细胞表面糖蛋白（主要是 CD45）的直接结合引起的，并且通过 c-Maf/芳香烃受体途径增强了 IL-21 的表达，这与 APC 无关。Gal-1 诱导的 IL-10(+)T 细胞有效抑制了 T 细胞增殖和 T 细胞介导的炎症，并促进了癌症免疫特权部位的建立。总的来说，这些发现表明 Gal-1 如何作为调节 Th 细胞发育、炎症和肿瘤免疫的主要聚糖决定因素发挥作用。
