The mer receptor tyrosine kinase: expression and function suggest a role in innate immunity
The mer receptor tyrosine kinase: expression and function suggest a role in innate immunity
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DOI：
10.1002/eji.200324076
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发表时间：
2003-08-01
影响因子：
5.4
通讯作者：
Cohen, PL
中科院分区：
文献类型：
--
作者：
Behrens, EM;Gadue, P;Cohen, PL
mer受体酪氨酸激酶介导凋亡细胞的吞噬作用并调节细胞因子的产生；它也是预防系统性自身免疫性疾病所必需的。使用 mer 特异性抗体，我们已经证实巨噬细胞上存在 mer，现在报告了其在 NK 细胞、NKT 细胞和树突状细胞 (DC) 上的表达。我们发现 DC 不需要 mer 来摄取凋亡细胞，因为来自 mer 缺陷小鼠的 DC 可以正常吞噬凋亡细胞。在脾脏切片中滤泡区域外的细胞上观察到 Mer，可能代表 DC 和巨噬细胞。 Mer 显然参与了 NKT 细胞抗原诱导的信号传导，因为来自 mer 缺陷小鼠的 NKT 细胞在体内 α-半乳糖神经酰胺刺激后表现出低得多的细胞因子产生；这种缺陷是 mer 缺陷型 NKT 细胞所固有的。总而言之，这些研究表明先天免疫系统细胞上有 mer 表达。 Mer 通过与脂质抗原的结合，不仅可以介导凋亡细胞的摄取，还可以在 NK 细胞、NKT 细胞和 DC 中发出信号事件。
The mer receptor tyrosine kinase mediates phagocytosis of apoptotic cells and modulates cytokine production; it is also required for prevention of systemic autoimmune disease. Using a mer-specific antibody, we have confirmed the presence of mer on macrophages and now report its expression on NK cells, NKT cells, and dendritic cells (DC). We found that DC do not require mer for ingestion of apoptotic cells, as DC from mer-deficient mice phagocytose apoptotic cells normally. Mer was observed in splenic sections on cells outside follicular areas, probably representing DC and macrophages. Mer apparently participates in NKT-cell antigen-induced signaling, as NKT cells from mer-deficient mice evinced much lower cytokine production after in vivo alpha-galactosylceramide stimulation; this defect was intrinsic to the mer-deficient NKT cells. Taken together, these studies show mer expression on cells of the innate immune system. Mer, through its binding of lipid antigens, may not only mediate ingestion of apoptotic cells, but also signal events in NK cells, NKT cells, and DC.