CD3+ cells transfer the hypersensitive granulomatous response to mycobacterial glycolipid trehalose 6,6'-dimycolate in mice.

摘要: The granulomatous response is the characteristic histological feature of Mycobacterium tuberculosis infection that essential for organism containment. Trehalose 6,6-dimycolate (TDM), a cell-wall glycolipid present on most mycobacterial species, has been implicated in pathogenesis M. infection. TDM potent immunoregulatory and inflammatory properties, can be used to model reactions mimic, part, pathology caused during active This study examined hypersensitive response, focusing cellular responses specific TDM. Lungs from mice immunized with emulsion demonstrated exacerbated damage, inflammation, lymphocytic infiltration upon subsequent challenge Splenocytes recovered these significant interferon (IFN)-γ production recall TDM, as well increased proinflammatory mediators (tumour necrosis factor-α, interleukin-6 macrophage protein-1α). could adoptively transferred naive mice. Administration non-adherent lymphocytes or purified CD3+ cells TDM-immunized led infiltration, vascular endothelial cell damage Recipient received increases Th1-type cytokines lung tissue following challenge. When CD1d−/− were they failed generate IFN-γ suggesting role this molecule generation hypersensitivity. These experiments provide further evidence involvement TDM-specific T pathological elicited