Department of Molecular Biology and Immunology and Institute for Cancer Research, University of North Texas Health Science Center, Fort Worth, TX 76107-2699, USA.
Clin Exp Immunol. 2010 Jun;160(3):348-58. doi: 10.1111/j.1365-2249.2010.04116.x. Epub 2010 Mar 16.
CS1 (CRACC, CD319) and 2B4 (CD244), members of the signalling lymphocyte activation molecule (SLAM) family receptors, regulate various immune functions. Genes encoding SLAM family receptors are located at 1q23, implicated in systemic lupus erythematosus (SLE). In this study, we have investigated the expression and alternative splicing of CS1 and 2B4 in immune cells from SLE patients. The surface expression of CS1 and 2B4 on total peripheral blood mononuclear cells (PBMCs), T, B, natural killer (NK) cells and monocytes in 45 patients with SLE and 30 healthy individuals was analysed by flow cytometry. CS1-positive B cell population was increased significantly in SLE patients. Because CS1 is a self-ligand and homophilic interaction of CS1 induces B cell proliferation and autocrine cytokine secretion, this could account for autoreactive B cell proliferation in SLE. The proportion of NK cells and monocytes expressing 2B4 on their surface was significantly lower in patients with SLE compared to healthy controls. Our study demonstrated altered expression of splice variants of CS1 and 2B4 that mediate differential signalling in PBMC from patients with SLE.
CS1（CRACC、CD319）和 2B4（CD244）是信号淋巴细胞激活分子（SLAM）家族受体的成员，调节各种免疫功能。编码 SLAM 家族受体的基因位于 1q23，与系统性红斑狼疮（SLE）有关。在这项研究中，我们研究了 SLE 患者免疫细胞中 CS1 和 2B4 的表达和选择性剪接。通过流式细胞术分析了 45 例 SLE 患者和 30 例健康个体外周血单个核细胞（PBMC）、T、B、自然杀伤（NK）细胞和单核细胞表面的 CS1 和 2B4 表达。SLE 患者中 CS1 阳性 B 细胞群体显著增加。因为 CS1 是自身配体，CS1 的同源相互作用诱导 B 细胞增殖和自分泌细胞因子分泌，这可能导致 SLE 中的自身反应性 B 细胞增殖。与健康对照组相比，SLE 患者 NK 细胞和单核细胞表面表达 2B4 的比例显著降低。我们的研究表明，SLE 患者 PBMC 中 CS1 和 2B4 的剪接变体表达发生改变，从而介导不同的信号转导。
