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急性猴免疫缺陷病毒感染期间肠道 CD4+和 CD8+T 细胞细胞因子/趋化因子反应的动力学。

Dynamics of cytokine/chemokine responses in intestinal CD4+ and CD8+ T Cells during Acute Simian Immunodeficiency Virus Infection.

机构信息

Division of Comparative Pathology, Tulane National Primate Research Center, Covington, Louisiana, USA.

出版信息

J Virol. 2013 Nov;87(21):11916-23. doi: 10.1128/JVI.01750-13. Epub 2013 Aug 21.

DOI:10.1128/JVI.01750-13
PMID:23966391
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3807351/
Abstract

Loss of intestinal CD4(+) T cells was associated with decreased production of several T-helper 1 (TH1) and TH2 cytokines and increased production of interleukin 17 (IL-17), gamma interferon (IFN-γ), CCL4, and granulocyte-macrophage colony-stimulating factor (GM-CSF) by CD8(+) T cells 21 days after simian immunodeficiency virus (SIV) infection in rhesus macaques. Shifting of mucosal TH1 to TH2 or T-cytotoxic 1 (TC1) to TC2 cytokine profiles was not evident. Additionally, both CD4(+) and CD8(+) T cells showed upregulation of macrophage migration inhibition factor (MIF) and basic fibroblast growth factor (FGF-basic) cytokines that have been linked to HIV disease progression.

摘要

感染猴免疫缺陷病毒（SIV）21 天后，肠道 CD4(+)T 细胞减少与 CD8(+)T 细胞产生的几种辅助性 T 细胞 1（TH1）和 TH2 细胞因子减少，白细胞介素 17（IL-17）、γ干扰素（IFN-γ）、趋化因子 CCL4 和粒细胞-巨噬细胞集落刺激因子（GM-CSF）增加有关。在恒河猴中，黏膜 TH1 向 TH2 或 T 细胞毒性 1（TC1）向 TC2 细胞因子谱的转变并不明显。此外，CD4(+)和 CD8(+)T 细胞均表现出巨噬细胞移动抑制因子（MIF）和碱性成纤维细胞生长因子（FGF-basic）细胞因子的上调，这些细胞因子与 HIV 疾病进展有关。

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