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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 >Absence of PI3Kgamma leads to increased leukocyte apoptosis and diminished severity of experimental autoimmune encephalomyelitis.
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Absence of PI3Kgamma leads to increased leukocyte apoptosis and diminished severity of experimental autoimmune encephalomyelitis.

机译：PI3Kgamma的缺乏会导致白细胞凋亡增加，并降低实验性自身免疫性脑脊髓炎的严重程度。

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摘要

Phosphatidylinositol-3-kinase gamma (PI3Kgamma) plays an important role in the motility of leukocytes in several models of inflammation. In this work, the role of PI3Kgamma in experimental autoimmune encephalomyelitis (EAE) was investigated. EAE was induced in wild-type and PI3Kgamma deficient mice (PI3Kgamma(-)(/)(-)). WT animals had a peak of clinical symptoms around day 14 post-induction (p.i.). PI3Kgamma(-)(/)(-) animals developed milder EAE signs and peak of disease was noticed only on day 21 p.i. Better clinical outcome correlated with the absence of perivascular cuffs on day 14 p.i. and with decreased levels of CCL2 and CCL5 in brain of PI3Kgamma(-)(/)(-) mice. There was increased leukocyte rolling and adhesion in pial vessels, as assessed by intravital microscopy, at day 14 after EAE induction in WT mice. The latter parameters were unaltered in PI3Kgamma(-)(/)(-) mice subjected to EAE. Moreover, the PI3Kgamma inhibitor AS-605240 given just before the intravital microscopy failed to affect leukocyte rolling or adhesion. Finally, there was a significant increase in the number of apoptotic cells in the CNS of EAE-induced PI3Kgamma(-/-) mice. Our results suggest that PI3Kgamma is involved in EAE and plays a more important role in mediating leukocyte survival than leukocyte adhesion in this experimental model of multiple sclerosis.
机译：在几种炎症模型中，磷脂酰肌醇-3-激酶γ（PI3Kgamma）在白细胞运动中起重要作用。在这项工作中，PI3Kgamma在实验性自身免疫性脑脊髓炎（EAE）中的作用进行了调查。在野生型和PI3Kgamma缺陷小鼠（PI3Kgamma（-）（/）（-））中诱导EAE。在诱导后第14天（p.i.），野生型动物的临床症状达到峰值。 PI3Kgamma（-）（/）（-）动物出现了较轻的EAE体征，仅在第21天p.i才注意到疾病高峰。较好的临床结果与p.i第14天没有血管周套扎有关。并且在PI3Kgamma（-）（/）（-）小鼠的大脑中CCL2和CCL5的水平降低。通过活体显微镜检查评估，WT小鼠EAE诱导后第14天，白内障血管白细胞滚动和粘附增加。在经历EAE的PI3Kgamma（-）（/）（-）小鼠中，后者的参数没有改变。此外，在活体内显微镜检查之前给予的PI3Kgamma抑制剂AS-605240无法影响白细胞滚动或粘连。最后，EAE诱导的PI3Kgamma（-/-）小鼠中枢神经系统的凋亡细胞数量显着增加。我们的结果表明，在这种多发性硬化的实验模型中，PI3Kgamma参与了EAE，并且在介导白细胞存活方面比白细胞粘附起着更重要的作用。

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