Increased susceptibility of mice lacking T-bet to infection with Mycobacterium tuberculosis correlates with increased IL-10 and decreased IFN-γ production

Brandon M. Sullivan, Ousman Jobe, Vanja Lazarevic, Kristine Vasquez, Roderick Bronson, Laurie H. Glimcher, Igor Kramnik

Research output: Contribution to journalArticlepeer-review

101 Scopus citations

Abstract

A sustained CD4+ Th1-dominated type 1 immune response is required to successfully control Mycobacterium tuberculosis infection. Considerable work has demonstrated that the transcription factor, T-bet, is required for IFN-γ expression and fundamental to the generation of type 1 immunity in multiple cell types. Mice lacking T-bet are susceptible to virulent M. tuberculosis infection. Susceptibility of T-bet-deficient mice is associated with increased systemic bacterial burden, diminished IFN-γ production, and the striking accumulation of eosinophilic macrophages and multinucleated giant cells in the lung. Interestingly, T-bet-/- mice did not develop a fully polarized Th2 response toward M. tuberculosis, but exhibited selective elevation of IL-10 production. These results indicate that T-bet plays a central role in controlling M. tuberculosis disease progression, in part through the regulation of both IFN-γ and IL-10.

Original languageEnglish
Pages (from-to)4593-4602
Number of pages10
JournalJournal of Immunology
Volume175
Issue number7
DOIs
StatePublished - 1 Oct 2005
Externally publishedYes

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