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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Acute stress impairs NK cell adhesion and cytotoxicity through CD2, but not LFA-1.
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Acute stress impairs NK cell adhesion and cytotoxicity through CD2, but not LFA-1.

机译：急性应激会通过CD2而不是LFA-1损害NK细胞的黏附和细胞毒性。

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摘要

Using a nonhuman primate model, we examined the mechanisms by which acute social stress inhibits the ability of NK cells to form conjugates with, and lyse target cells. We examined the expression and role of the primary NK cell adhesion molecules, CD2 and LFA-1, in mediating conjugation to target cells. Acute stress induced a decrease in NK cell expression of CD2 (17+/-3%); and to a lesser degree induced a decrease in expression of LFA-1 (CD11a: 8+/-3%; CD18: 7+/-3%). Antibody blocking studies indicated that anti-LFA-1 significantly inhibited NK cell conjugate formation and cytotoxicity in both control (approximately 40% and approximately 50%, respectively) and stressed (approximately 20% and approximately 45%, respectively) conditions. However, anti-CD2 blocked conjugation and cytotoxicity in the control condition by approximately 50%, but had no capacity to further affect the inhibition of conjugation or cytotoxicity of NK cells induced by acute stress. These data indicate that there are differential effects of acute stress on the expression and function of LFA-1 and CD2, and that the stress-induced inhibition of NK cell adhesion and cytotoxicity is dependent upon modulation of adhesion and/or signalling through CD2.
机译：使用非人类的灵长类动物模型，我们研究了急性社会压力抑制NK细胞与目标细胞形成结合物并裂解目标细胞的能力的机制。我们检查了主要的NK细胞粘附分子CD2和LFA-1的表达及其在介导与靶细胞结合中的作用。急性应激诱导NK细胞CD2表达降低（17 +/- 3％）;并在较小程度上诱导LFA-1表达下降（CD11a：8 +/- 3％; CD18：7 +/- 3％）。抗体阻断研究表明，抗-LFA-1在对照（分别约为40％和50％）和应激（分别约为20％和45％）条件下均能显着抑制NK细胞共轭物的形成和细胞毒性。然而，抗CD2在对照条件下阻断了缀合和细胞毒性约50％，但是没有能力进一步影响对急性应激诱导的NK细胞的缀合或细胞毒性的抑制。这些数据表明，急性应激对LFA-1和CD2的表达和功能有不同的影响，并且应激诱导的NK细胞粘附和细胞毒性的抑制作用取决于对粘附的调节和/或通过CD2的信号传导。

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