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

• Autor(a) principal: Cruz, Andrea
• Data de Publicação: 2006
• Outros Autores: Khader, Shabaana A., Torrado, Egídio, Fraga, Alexandra G., Pearl, John E., Pedrosa, Jorge, Cooper, Andrea M., Castro, António G.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/1822/5342
• topic: IFN-alpha; IL-17; CD4 T Cells; Mycobacterial Infection; Science & Technology

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 Gue´rin. Furthermore, exogenous IFN-γ increases IL-12 and decreases IL-23 production by bacille Calmette Gue´rin-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.