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白细胞介素-10受体阻断后慢性病毒感染的消退

Resolution of a chronic viral infection after interleukin-10 receptor blockade.

作者信息

Ejrnaes Mette, Filippi Christophe M, Martinic Marianne M, Ling Eleanor M, Togher Lisa M, Crotty Shane, von Herrath Matthias G

机构信息

Immune Regulation Lab - DI3, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.

出版信息

J Exp Med. 2006 Oct 30;203(11):2461-72. doi: 10.1084/jem.20061462. Epub 2006 Oct 9.

DOI:10.1084/jem.20061462
PMID:17030951
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2118120/
Abstract

A defining characteristic of persistent viral infections is the loss and functional inactivation of antiviral effector T cells, which prevents viral clearance. Interleukin-10 (IL-10) suppresses cellular immune responses by modulating the function of T cells and antigen-presenting cells. In this paper, we report that IL-10 production is drastically increased in mice persistently infected with lymphocytic choriomeningitis virus. In vivo blockade of the IL-10 receptor (IL-10R) with a neutralizing antibody resulted in rapid resolution of the persistent infection. IL-10 secretion was diminished and interferon gamma production by antiviral CD8+ T cells was enhanced. In persistently infected mice, CD8alpha+ dendritic cell (DC) numbers declined early after infection, whereas CD8alpha- DC numbers were not affected. CD8alpha- DCs supported IL-10 production and subsequent dampening of antiviral T cell responses. Therapeutic IL-10R blockade broke the cycle of IL-10-mediated immune suppression, preventing IL-10 priming by CD8alpha- DCs and enhancing antiviral responses and thereby resolving infection without causing immunopathology.

摘要

持续性病毒感染的一个决定性特征是抗病毒效应T细胞的丧失和功能失活，这会阻止病毒清除。白细胞介素-10（IL-10）通过调节T细胞和抗原呈递细胞的功能来抑制细胞免疫反应。在本文中，我们报告在持续感染淋巴细胞性脉络丛脑膜炎病毒的小鼠中，IL-10的产生急剧增加。用中和抗体在体内阻断IL-10受体（IL-10R）可导致持续性感染迅速消退。IL-10分泌减少，抗病毒CD8 + T细胞产生的干扰素γ增加。在持续感染的小鼠中，感染后早期CD8α +树突状细胞（DC）数量下降，而CD8α - DC数量未受影响。CD8α - DC支持IL-10的产生以及随后对抗病毒T细胞反应的抑制。治疗性IL-10R阻断打破了IL-10介导的免疫抑制循环，阻止了CD8α - DC引发的IL-10，并增强了抗病毒反应，从而在不引起免疫病理的情况下解决感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/2861f2a38329/jem2032461f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/c6f6663c8897/jem2032461f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/2da77edb5fa6/jem2032461f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/eb3e4acd0e5d/jem2032461f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/e409da951c33/jem2032461f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/2861f2a38329/jem2032461f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/c6f6663c8897/jem2032461f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/2da77edb5fa6/jem2032461f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/eb3e4acd0e5d/jem2032461f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/e409da951c33/jem2032461f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d50/2118120/2861f2a38329/jem2032461f05.jpg

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