TLR2型
Toll样受体
基因亚型
生物
信号转导衔接蛋白
细胞生物学
受体
信号转导
分子生物学
转染
TLR4型
先天免疫系统
细胞培养
生物化学
基因
遗传学
作者
Ankita Srivastava,Arathi Nair,Surya Prakash Pandey,George Eduardo Gabriel Kluck,Inês Mesquita,Tithi Ghosh,Anamika Bose,Rathindranath Baral,Ricardo Silvestre,Neelam Bodhale,Bhaskar Saha
出处
期刊:Cytokine
[Elsevier]
日期:2023-07-28
卷期号:169: 156301-156301
被引量:2
标识
DOI:10.1016/j.cyto.2023.156301
摘要
Leishmania infection of macrophages results in altered Ras isoforms expression and Toll-like receptor-2 (TLR2) expression and functions. Therefore, we examined whether TLR2 would selectively alter Ras isoforms' expression in macrophages. We observed that TLR2 ligands- Pam3CSK4, peptidoglycan (PGN), and FSL- selectively modulated the expression of Ras isoforms in BALB/c-derived elicited macrophages. Lentivirally-expressed TLR1-shRNA significantly reversed this Ras isoforms expression profile. TLR2-deficient L. major-infected macrophages and the lymph node cells from the L. major-infected mice showed similarly reversed Ras isoforms expression. Transfection of the macrophages with the siRNAs for the adaptors- Myeloid Differentiation factor 88 (MyD88) and Toll-Interleukin-1 Receptor (TIR) domain-containing adaptor protein (TIRAP)- or Interleukin-1 Receptor-Associated Kinases (IRAKs)- IRAK1 and IRAK4- significantly inhibited the L. major-induced down-regulation of K-Ras, and up-regulation of N-Ras and H-Ras, expression. The TLR1/TLR2-ligand Pam3CSK4 increased IL-10 and TGF-β expression in macrophages. Pam3CSK4 upregulated N-Ras and H-Ras, but down-regulated K-Ras, expression in C57BL/6 wild-type, but not in IL-10-deficient, macrophages. IL-10 or TGF-β signaling inhibition selectively regulated Ras isoforms expression. These observations indicate the specificity of the TLR2 regulation of Ras isoforms and their selective modulation by MyD88, TIRAP, and IRAKs, but not IL-10 or TGF-β, signaling.
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