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CC趋化因子配体3在中枢神经系统病毒感染后调节CD11c⁺CD11b⁺CD8α⁻树突状细胞的成熟和激活：对其在T细胞激活中的作用的启示

The CC chemokine ligand 3 regulates CD11c+CD11b+CD8alpha- dendritic cell maturation and activation following viral infection of the central nervous system: implications for a role in T cell activation.

作者信息

Trifilo Matthew J, Lane Thomas E

机构信息

Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697-3900, USA.

出版信息

Virology. 2004 Sep 15;327(1):8-15. doi: 10.1016/j.virol.2004.06.027.

DOI:10.1016/j.virol.2004.06.027
PMID:15327893
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7111789/
Abstract

The role of CC chemokine ligand 3 (CCL3) in activation of dendritic cells (DCs) following mouse hepatitis virus (MHV) infection of the central nervous system (CNS) was examined. The results indicate that CCL3 participates in an effective host response to MHV infection by contributing to CD11c+CD11b+CD8alpha- DC maturation, activation, and migration to cervical lymph nodes (CLN). Diminished CD8alpha- DC activation correlated with reduced IFN-gamma expression by virus-specific T cells accompanied by increased IL-10 production suggesting that CCL3 contributes to an effective host response to viral infection by enhancing the T cell activation potential of DC.

摘要

研究了CC趋化因子配体3（CCL3）在小鼠肝炎病毒（MHV）感染中枢神经系统（CNS）后对树突状细胞（DC）激活中的作用。结果表明，CCL3通过促进CD11c+CD11b+CD8α-DC的成熟、激活以及向颈淋巴结（CLN）迁移，参与宿主对MHV感染的有效应答。CD8α-DC激活减弱与病毒特异性T细胞产生的IFN-γ表达降低相关，同时IL-10产生增加，这表明CCL3通过增强DC的T细胞激活潜能，促进宿主对病毒感染的有效应答。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e7/7111789/c3bb4d361c93/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e7/7111789/d4f5da5ee3cd/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e7/7111789/5e20623121ce/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e7/7111789/c3bb4d361c93/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e7/7111789/d4f5da5ee3cd/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e7/7111789/5e20623121ce/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e7/7111789/c3bb4d361c93/gr3.jpg

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