GSBS Student Publications

Student Author(s)

Jenny Wun-Yue Che

GSBS Program

Immunology & Microbiology

UMMS Affiliation

Department of Pathology

Date

2-1-2015

Document Type

Article

Medical Subject Headings

Animals; *Apoptosis; Arenaviridae Infections; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cell Survival; Gene Expression Regulation; Interferon Type I; Interleukin-7; Lymphocytic choriomeningitis virus; Mice, Inbred C57BL; T-Lymphocytes, Regulatory

Disciplines

Allergy and Immunology | Immunology and Infectious Disease | Immunology of Infectious Disease | Immunopathology | Microbiology | Virology | Virus Diseases

Abstract

Regulatory T (Treg) cells are important in the maintenance of self-tolerance, and the depletion of Treg cells correlates with autoimmune development. It has been shown that type I interferon (IFN) responses induced early in the infection of mice can drive memory (CD44hi) CD8 and CD4 T cells into apoptosis, and we questioned here whether the apoptosis of CD44-expressing Treg cells might be involved in the infection-associated autoimmune development. Instead, we found that Treg cells were much more resistant to apoptosis than CD44hi CD8 and CD4 T cells at days 2 to 3 after lymphocytic choriomeningitis virus infection, when type I IFN levels are high. The infection caused a downregulation of the interleukin-7 (IL-7) receptor, needed for survival of conventional T cells, while increasing on Treg cells the expression of the high-affinity IL-2 receptor, needed for STAT5-dependent survival of Treg cells. The stably maintained Treg cells early during infection may explain the relatively low incidence of autoimmune manifestations among infected patients.

IMPORTANCE: Autoimmune diseases are controlled in part by regulatory T cells (Treg) and are thought to sometimes be initiated by viral infections. We tested the hypothesis that Treg may die off at early stages of infection, when virus-induced factors kill other lymphocyte types. Instead, we found that Treg resisted this cell death, perhaps reducing the tendency of viral infections to cause immune dysfunction and induce autoimmunity.

Rights and Permissions

Citation: J Virol. 2015 Feb;89(4):2112-20. doi: 10.1128/JVI.02245-14. Epub 2014 Dec 3. Link to article on publisher's site

DOI of Published Version

10.1128/JVI.02245-14

Comments

Copyright © 2015, American Society for Microbiology. All Rights Reserved. Publisher PDF posted as allowed by the publisher's author rights policy at http://journals.asm.org/site/misc/ASM_Author_Statement.xhtml.

Related Resources

Link to Article in PubMed

Journal Title

Journal of virology

PubMed ID

25473049

 
 

To view the content in your browser, please download Adobe Reader or, alternately,
you may Download the file to your hard drive.

NOTE: The latest versions of Adobe Reader do not support viewing PDF files within Firefox on Mac OS and if you are using a modern (Intel) Mac, there is no official plugin for viewing PDF files within the browser window.