The development and function of memory regulatory T cells after acute viral infections

Natural CD4+CD25+Foxp3+ regulatory T cells (Tregs) are critical for the control of immune responses to pathogens. However, most studies have focused on chronic infections, in which pathogen-specific Tregs contribute to pathogen persistence and, in some cases, concomitant immunity. How Tregs behave a...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of immunology (1950) 2012-09, Vol.189 (6), p.2805-2814
Main Authors: Sanchez, Ana M, Zhu, Jiangao, Huang, Xiaopei, Yang, Yiping
Format: Article
Language:English
Subjects:
Acute Disease
Adenoviridae - immunology
Animals
Gene Knock-In Techniques
Hemagglutinins - biosynthesis
Hemagglutinins - immunology
Immunologic Memory - genetics
Influenza A virus - immunology
Interleukin-10 - physiology
Lymphocyte Activation - immunology
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Transgenic
T-Lymphocytes, Regulatory - immunology
T-Lymphocytes, Regulatory - metabolism
T-Lymphocytes, Regulatory - virology
Vaccinia virus - genetics
Vaccinia virus - immunology
Vaccinia virus - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Natural CD4+CD25+Foxp3+ regulatory T cells (Tregs) are critical for the control of immune responses to pathogens. However, most studies have focused on chronic infections, in which pathogen-specific Tregs contribute to pathogen persistence and, in some cases, concomitant immunity. How Tregs behave and function following acute infections remains largely unknown. In this article, we show that pathogen-specific Tregs can be activated and expand upon acute viral infections in vivo. The activated Tregs then contract to form a memory pool after resolution of the infection. These memory Tregs expand rapidly upon a secondary challenge, secrete large amounts of IL-10, and suppress excessive immunopathological conditions elicited by recall expansion of non-Tregs via an IL-10-dependent mechanism. Our work reveals a memory Treg population that develops after acute viral infections and may help in the design of effective strategies to circumvent excessive immunopathological effects.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.1200645