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首页> 外文期刊>Journal of Cellular Physiology >Effect of lysophospholipids on signaling in the human Jurkat T cell line.
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Effect of lysophospholipids on signaling in the human Jurkat T cell line.

机译：溶血对信号的影响人类Jurkat T细胞系。

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Lysophospholipids have recently been demonstrated to induce activation and proliferation of fibroblasts and other cell lineages by interacting with high affinity cell surface receptors leading to specific intracellular signaling events. Platelet activation, likely at the site of injury or inflammation, results in increased production of lysophospholipids suggesting a possible source of lysophospholipids. We have recently demonstrated that high concentrations of lysophospholipids are present in ascites and plasma from ovarian cancer patients, suggesting that physiologically produced lysophospholipids could interact with cells present in these fluids, including lymphocytes, and alter their function. We demonstrate herein that lysophosphatidic acid (LPA), lysophosphatidylserine (LPS), and sphingosylphosphorylcholine (SPC) activate the Jurkat T cell line. Each of the lysophospholipids induced a transient increase in cytosolic free calcium ([Ca2+]i) in Jurkat cells. Increases in [Ca2+]i were cross-desensitized by LPA, LPS and SPC, suggesting that the lysophospholipids share the same receptor(s) or that their downstream signaling pathways converge or interact. Lysophosphatidylglycerol (LPG), a competitive inhibitor of the putative LPA receptor, inhibited the calcium releasing activity of LPA, but not that of LPS and SPC, suggesting that these lysophospholipids interact with different receptors and that desensitization is due to interactions in downstream signaling pathways. The ability of the lysophospholipids to induce increases in [Ca2+]i was attenuated, but not completely blocked, by increases in [Ca2+]i induced by activation of the thrombin receptor. In contrast, increases in [Ca2+]i induced by the lysophospholipids and cross-linking the CD3 component of the T cell receptor complex with the UCHT1 antibody did not undergo heterologous desensitization. Strikingly, LPA is sufficient to stimulate proliferation of Jurkat cells in serum-free medium or in synergy with low concentrations of fetal bovine serum. In addition, LPA also increased the production of the T cell growth factor, interleukin 2 (IL-2), by Jurkat cells treated with phorbol esters. LPS, in contrast, inhibited Jurkat proliferation while increasing IL-2 production and SPC inhibited both processes. Thus, although all three lysophospholipids were sufficient to induce a transient increase in [Ca2+]i in Jurkat cells, they induced markedly different physiological consequences.
机译：溶血磷脂最近被证实诱导激活和扩散成纤维细胞和其他细胞谱系与高亲和力细胞表面相互作用受体导致特定的细胞内信号事件。损伤或炎症、结果的网站增加产量的溶血磷脂暗示的可能来源溶血磷脂。高浓度的溶血在从卵巢癌腹水和血浆病人,表明生理上溶血可能与生产细胞存在于这些液体,包括淋巴细胞,并改变其功能。在此证明lysophosphatidic酸sphingosylphosphorylcholine (SPC)激活Jurkat T细胞系。感应瞬态增加胞质自由钙([Ca2 +] i) Jurkat细胞。[Ca2 +]我是cross-desensitized LPA,有限合伙人SPC,表明溶血份额相同的受体(s)或他们的下游信号通路收敛或交互。Lysophosphatidylglycerol(液化石油气)竞争假定的LPA受体的抑制剂,抑制LPA的钙释放活动,但不是有限合伙人和SPC,说明这些溶血磷脂与不同受体脱敏是由于相互作用在下游信号通路。引起的溶血磷脂的能力增加[Ca2 +]我减毒,但不是完全阻塞,增加在[Ca2 +]我由凝血酶受体的激活。相比之下,增加[Ca2 +]我引发的溶血磷脂和CD3交联组件的T细胞受体复杂UCHT1抗体不接受不齐的脱敏。刺激Jurkat细胞扩散无血清培养基或在较低的协同作用胎牛血清的浓度。此外,LPA也增加了生产T细胞生长因子、白介素2 (- 2),Jurkat细胞接受佛波醇酯。相比之下,抑制Jurkat扩散增加生产和SPC - 2抑制流程。溶血是足以引起瞬态[Ca2 +]我增加Jurkat细胞,他们诱导显著不同的生理的后果。

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