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CD4C/人类免疫缺陷病毒转基因小鼠的艾滋病样疾病与未成熟CD11bHi树突状细胞的积累有关。

The AIDS-like disease of CD4C/human immunodeficiency virus transgenic mice is associated with accumulation of immature CD11bHi dendritic cells.

作者信息

Poudrier Johanne, Weng Xiaoduan, Kay Denis G, Hanna Zaher, Jolicoeur Paul

机构信息

Laboratory of Molecular Biology, Clinical Research Institute of Montréal, Montréal, Québec H2W 1R7, Canada.

出版信息

J Virol. 2003 Nov;77(21):11733-44. doi: 10.1128/jvi.77.21.11733-11744.2003.

DOI:10.1128/jvi.77.21.11733-11744.2003
PMID:14557658
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC229375/
Abstract

CD4C/human immunodeficiency virus (HIV) transgenic mice develop an AIDS-like disease. We used this model to study the effects of HIV-1 on dendritic cells (DC). We found a progressive decrease in total DC numbers in the lymph nodes, with a significant accumulation of CD11b(Hi) DC. In the thymus, the recovery of transgenic CD8alpha(+) DC had a tendency to be lower. Spleen DC were augmented in the marginal zone. Transgenic DC showed a decreased capacity to present antigen in vitro, consistent with their reduced major histocompatibility complex class II expression and impaired maturation profile. The accumulation of immature DC may contribute to disease and may reflect an adaptive advantage for the virus by favoring its replication and preventing the generation of fully functional antiviral responses.

摘要

CD4C/人类免疫缺陷病毒（HIV）转基因小鼠会发展出类似艾滋病的疾病。我们利用这个模型来研究HIV-1对树突状细胞（DC）的影响。我们发现淋巴结中DC总数逐渐减少，CD11b（高表达）DC显著积聚。在胸腺中，转基因CD8α（+）DC的恢复趋势较低。脾脏DC在边缘区增多。转基因DC在体外呈现抗原的能力下降，这与其主要组织相容性复合体II类表达降低和成熟谱受损一致。未成熟DC的积聚可能导致疾病，并且可能通过有利于病毒复制和阻止产生完全功能性的抗病毒反应而反映出病毒的适应性优势。

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