Microbial infection-induced expansion of effector T cells overcomes the suppressive effects of regulatory T cells via an IL-2 deprivation mechanism

Alicia Benson, Sean Murray, Prashanthi Divakar, Nikolay Burnaevskiy, Reed Pifer, James Forman, Felix Yarovinsky

Research output: Contribution to journalArticlepeer-review

53 Scopus citations

Abstract

Foxp3 + regulatory T (Treg) cells are a critical cell population that suppresses T cell activation in response to microbial and viral pathogens. We identify a cell-intrinsic mechanism by which effector CD4 + T cells overcome the suppressive effects of Treg cells in the context of three distinct infections: Toxoplasma gondii, Listeria monocytogenes, and vaccinia virus. The acute responses to the parasitic, bacterial, and viral pathogens resulted in a transient reduction in frequency and absolute number of Treg cells. The infection-induced partial loss of Treg cells was essential for the initiation of potent Th1 responses and host protection against the pathogens. The observed disappearance of Treg cells was a result of insufficiency in IL-2 caused by the expansion of pathogen-specific CD4 + T cells with a limited capacity of IL-2 production. Exogenous IL-2 treatment during the parasitic, bacterial, and viral infections completely prevented the loss of Treg cells, but restoration of Treg cells resulted in a greatly enhanced susceptibility to the pathogens. These results demonstrate that the transient reduction in Treg cells induced by pathogens via IL-2 deprivation is essential for optimal T cell responses and host resistance to microbial and viral pathogens.

Original languageEnglish (US)
Pages (from-to)800-810
Number of pages11
JournalJournal of Immunology
Volume188
Issue number2
DOIs
StatePublished - Jan 15 2012

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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