IL-6 is not Absolutely Essential for the Development of a TH17 Immune Response after an Aerosol Infection with Mycobacterium Tuberculosis H37rv.

摘要: Anti-inflammatory treatment of chronic inflammatory diseases often increases susceptibility to infectious such as tuberculosis (TB). Since numerous and autoimmune are mediated by interleukin (IL)-6-induced T helper (TH) 17 cells, a TH17-directed anti-inflammatory therapy may be preferable an IL-12-dependent TH1 inhibition in order avoid reactivation latent infections. To assess, however, the risk IL-6-dependent TH17-mediated inflammation, we examined TH17 immune response course experimental TB IL-6- T-cell-specific gp130-deficient mice. Our study revealed that absence IL-6 or gp130 on cells has only minor effect development antigen-specific cells. Importantly, these gene-deficient mice were capable wild type control mycobacterial infection. Together, contrast its key function for other diseases, plays inferior role generation responses during TB.