组织等离子素激活剂对急性炎症中骨髓状细胞表型的影响

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Célia Seillier¹, Léonie Lesec¹, Pauline Hélie^1,2

¹Institut Blood and Brain @Caen-Normandie (BB@C), UMR-S U1237, Physiopathology and Imaging of Neurological Disorders (PhIND), Normandie Univ, UNICAEN, INSERM, GIP Cyceron, Caen, France.

Journal of inflammation (London, England)

|February 14, 2024

概括

组织等离子素激活剂 (tPA) 在炎症期间影响髓状细胞表型. tPA 缺乏会改变巨细胞和树突细胞对脂聚糖 (LPS) 的反应,影响适应性免疫力.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

组织等离子素激活剂 (tPA),一种血清蛋白酶,已知用于纤维素分解.
新兴的体外证据表明,tPA通过产生等离子体或受体信号来调节炎症.
在体内tPA在炎症过程中的作用仍然不完全理解.

研究的目的:

调查tPA在体内对炎症反应的贡献.
分析脂聚糖化物 (LPS) 挑战对tPA缺乏小鼠骨髓状细胞表型的影响.

主要方法:

使用的tPA缺乏 (tPA-/-) 和野生型 (WT) 鼠.
使用脂聚糖 (LPS) 诱导急性炎症.
在脏中使用流细胞计分析了髓状细胞群 (中性粒细胞,巨细胞,树突细胞).
评估了MHCII,CD11b和CD86分子的表达水平.

主要成果:

LPS上调MHCII+巨细胞,但矛盾的是,对巨细胞和cDC2s进行了下调MHCII.
作为tPA受体的CD11b整合素被LPS在MHCII+巨细胞和cDC2s上调节.
在tPA-/-小鼠中,MHCII+巨细胞上的CD86表达在炎症下降,而稳定状态MHCII则更高.
在急性炎症期间,tPA 缺乏稍微改变了DC和T细胞表型.

结论:

在活体中,LPS对巨细胞和DCs中的MHCII表达具有双模作用,可能会影响适应性免疫力.
在炎症期间,tPA可以通过调节巨细胞上的CD86和MHCII水平来调节T细胞反应.

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