Increased resistance to mycobacterial infection in the absence of interleukin-10.

摘要: Interleukin-10 (IL-10) down-regulates T helper type 1 cell and macrophage functions. As IL-10 is induced along with tumour necrosis factor (TNF) IL-12 in mycobacterial infection, we asked whether endogenous plays a role the antimycobacterial response. We demonstrate here that IL-10-deficient mice eliminate Mycobacterium bovis Calmette-Guerin bacillus faster than wild-type mice. Granulomas are significantly larger, containing more CD-11b- CD11c-positive antigen-presenting cells cells, expression of major histocompatibility complex class II intracellular adhesion molecule-1 increased. Macrophages granulomas express high levels TNF, acid phosphatase inducible nitric oxide synthase (iNOS). Finally, an increased cutaneous delayed-type hypersensitivity reaction to proteins further evidence augmented cell-mediated immune In conclusion, immunity enhanced absence IL-10, resulting robust granuloma response, which accelerates clearance mycobacteria. Therefore, attenuates immunity.