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母-胎界面的滋养细胞、蜕膜淋巴细胞和蜕膜基质均表达多种趋化因子及其受体。滋养细胞分泌的MIP-1α募集外周血中CD56brightNK细胞至母-胎界面;蜕膜血管表达SLC,特异性趋化CD56brightNK细胞。除募集蜕膜淋巴细胞外,母-胎界面的趋化因子及其受体尚参与固有免疫应答,并调节滋养细胞侵袭、分化及胎盘形成。滋养细胞固有表达CXCR4和CCR5,HIV-1利用CXCR4或CCR5入侵胎儿细胞,导致HIV-1经子宫垂直传播。滋养细胞及蜕膜细胞分泌的IL-8在炎症相关的早产中具有重要作用。
Trophoblastic, decidual lymphocytes and decidual matrix in the maternal-fetal interface both express a variety of chemokines and their receptors. MIP-1α secreted by trophoblasts recruits CD56brightNK cells from the peripheral blood to the maternal-fetal interface; SLC decidualized blood vessels specifically chemotactic to CD56brightNK cells. In addition to the recruitment of decidual lymphocytes, the maternal-fetal interface chemokines and their receptors are still involved in the innate immune response and regulate trophoblast invasion, differentiation and placental formation. Trophoblasts are inherently expressed in CXCR4 and CCR5, and HIV-1 invades fetal cells using CXCR4 or CCR5, resulting in vertical transmission of HIV-1 across the uterus. IL-8 secreted by trophoblasts and decidual cells plays an important role in inflammation-related preterm birth.