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To whom correspondence may be addressed. E-mail: eshevach@niaid.nih.gov or rahmed@emory.edu.

Contributed by Rafi Ahmed, January 10, 2011 (sent for review October 11, 2010)

Author contributions: G.A.P., J.P.D., R.A., and E.M.S. designed research; G.A.P., M.B., D.D.G., M.M.L., and L.O. performed research; G.A.P. analyzed data; and G.A.P. and E.M.S. wrote the paper.

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Research Funding:

This work was supported by the Intramural Research Program of the National Institutes of Health (NIH), NIAID, the Bill and Melinda Gates Foundation, and NIH Grant R01-CA116813.

Regulatory T-cell expansion during chronic viral infection is dependent on endogenous retroviral superantigens

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Journal Title:

Proceedings of the National Academy of Sciences

Volume:

Volume 108, Number 9

Publisher:

, Pages 3677-3682

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Regulatory T cells (Treg) play critical roles in the modulation of immune responses to infectious agents. Further understanding of the factors that control Treg activation and expansion in response to pathogens is needed to manipulate Treg function in acute and chronic infections. Here we show that chronic, but not acute, infection of mice with lymphocytic choriomeningitis virus results in a marked expansion of Foxp3+ Treg that is dependent on retroviral superantigen (sag) genes encoded in the mouse genome. Sag-dependent Treg expansion was MHC class II dependent, CD4 independent, and required dendritic cells. Thus, one unique mechanism by which certain infectious agents evade host immune responses may be mediated by endogenous Sag-dependent activation and expansion of Treg.

Copyright information:

Beginning with articles submitted in Volume 106 (2009) the author(s) retains copyright to individual articles, and the National Academy of Sciences of the United States of America retains an exclusive license to publish these articles and holds copyright to the collective work.

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