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*Tuberculosis
The Journal of Immunology, 2006, 177: 1416-1420.
Copyright © 2006 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: IFN-{gamma} Regulates the Induction and Expansion of IL-17-Producing CD4 T Cells during Mycobacterial Infection1

Andrea Cruz*, Shabaana A. Khader{dagger}, Egidio Torrado*, Alexandra Fraga*, John E. Pearl{dagger}, Jorge Pedrosa*, Andrea M. Cooper2,{dagger} and António G. Castro*

* Life and Health Sciences Research Institute, School of Health Sciences, University of Minho, Braga, Portugal; and {dagger} Trudeau Institute, Saranac Lake, NY 12983

T cell responses are important to the control of infection but are deleterious if not regulated. IFN-{gamma}-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-{gamma}-deficient mice have increased numbers of IL-17-producing T cells following infection with Mycobacterium bovis bacille Calmette Guérin. Furthermore, exogenous IFN-{gamma} 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-{gamma}- and IL-17-producing T cells are induced, but that IFN-{gamma} 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.




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