Cutting edge: IFN-γ regulates the induction and expansion of IL-17-producing CD4 T cells during mycobacterial infection

Andrea Cruz, Shabaana A. Khader, Egidio Torrado, Alexandra Fraga, John E. Pearl, Jorge Pedrosa, Andrea M. Cooper, António G. Castro

Research output: Contribution to journalArticlepeer-review

231 Scopus citations

Abstract

T cell responses are important to the control of infection but are deleterious if not regulated. IFN-γ-deficient mice infected with mycobacteria exhibit enhanced accumulation of activated effector T cells and neutrophils within granulomatous lesions. These cells do not control bacterial growth and compromise the integrity of the infected tissue. We show that IFN-γ-deficient mice have increased numbers of IL-17-producing T cells following infection with Mycobacterium bovis bacille Calmette Guérin. Furthermore, exogenous IFN-γ increases IL-12 and decreases IL-23 production by bacille Calmette Guérin-infected bone marrow-derived dendritic cells and reduces the frequency of IL-17-producing T cells induced by these bone marrow-derived dendritic cells. These data support the hypothesis that, during mycobacterial infection, both IFN-γ-and IL-17-producing T cells are induced, but that IFN-γ serves to limit the IL-17-producing T cell population. This counterregulation pathway may be an important factor in limiting mycobacterially associated immune-mediated pathology.

Original languageEnglish
Pages (from-to)1416-1420
Number of pages5
JournalJournal of Immunology
Volume177
Issue number3
DOIs
StatePublished - Aug 1 2006

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