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收费类受体2在莱什马尼亚主要感染中选择性调节Ras异型的表达

Ankita Srivastava¹, Arathi Nair¹, Surya P Pandey¹

¹National Centre for Cell Science, Ganeshkhind, Pune 411007, India.

|July 29, 2023

概括

收费类受体2 (TLR2) 信号在莱什马尼亚感染期间特别改变巨细胞中的Ras异型. 这种调制涉及骨髓区分因子88 (MyD88) 和IRAKs,但不涉及IL-10或TGF-β信号通路.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

莱什曼尼亚感染会影响巨细胞Ras和Toll类受体-2 (TLR2) 的表达.
TLR2在先天性免疫反应和巨细胞功能中起着至关重要的作用.

研究的目的:

调查TLR2是否有选择性调节巨细胞中Ras异型体的表达.
为了阐明涉及TLR2-介导的Ras异型调节在莱什曼尼亚感染期间的特定信号通路.

主要方法:

大细胞被TLR2连接体 (Pam3CSK4,PGN,FSL) 刺激.
拉斯异构体的表达被分析为MyD88,TIRAP,IRAK1和IRAK4的用lentiviral表达的TLR1-shRNA,TLR2-缺乏的巨细胞和siRNA转染.
评估了细胞因子表达 (IL-10,TGF-β) 和信号抑制.

主要成果:

在巨细胞中选择性调节的Ras异型 (K-Ras,N-Ras,H-Ras) 表达的TLR2配体.
通过TLR1的淘汰和TLR2的缺陷,可以逆转这些调节.
MyD88,TIRAP,IRAK1和IRAK4被确定为该途径中的关键适配器.
帕姆3CSK4诱导的Ras异型变化依赖于IL-10,但IL-10或TGF-β信号抑制没有直接调节Ras异型.

结论:

在莱什马尼亚感染期间,TLR2特别调节巨细胞中Ras异型体的表达.
调制依赖于MyD88,TIRAP和IRAKs的信号通路.
IL-10和TGF-β信号是下游的效应因子,而不是TLR2-介导的Ras异型变化的直接调节者.

关键词:

莱什曼尼亚 (Leishmania) 是一种病.脂酸盐可以是脂酸盐.巨细胞是一个巨细胞.拉斯是Ras的同位体.TLR信号传输系统的信号.

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