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CUTTING EDGE |
Regulates the Induction and Expansion of IL-17-Producing CD4 T Cells during Mycobacterial Infection1



* Life and Health Sciences Research Institute, School of Health Sciences, University of Minho, Braga, Portugal; and
Trudeau Institute, Saranac Lake, NY 12983
T cell responses are important to the control of infection but are deleterious if not regulated. IFN-
-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-
-deficient mice have increased numbers of IL-17-producing T cells following infection with Mycobacterium bovis bacille Calmette Guérin. Furthermore, exogenous IFN-
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-
- and IL-17-producing T cells are induced, but that IFN-
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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