Therefore, it is possible that these healthy individuals had been exposed to Mtb in their lifetime, and that this had caused the high production of IFN-γ after stimulation in vitro with PPD and H37Ra. More normal healthy individuals from non-endemic TB areas who have been confirmed negative CHIR-99021 mw by chest X-ray and TST, and tested for latent TB infection and infection manifesting as active TB by IGRAs, should be included in future studies. IFN-γ is produced from T cells (both CD4+

and CD8+T cells) and NK cells and activates bactericidal mechanisms in macrophages (3). It has been demonstrated that during the course of chronic and fatal TB infection, CD4+ T cells are absent even though CD8+ T cells can produce large amounts of IFN-γ. This supports the hypotheses that CD4+ T cells have important, non redundant roles in control of Mtb in addition to IFN-γ production, that CD4+ T cells assist in the development of cytotoxic CD8+ T cell populations and that the cytotoxicity exerted by effector LY294002 ic50 CD8+ T cells might be an important component of anti-mycobacterial immunity (22). The present results indicate that patients with newly diagnosed and relapsed TB have low circulating granulysin but high IFN-γ concentrations before anti-TB therapy, suggesting that granulysin and IFN-γ may act in concert or in synergy in host defense against Mtb infection. In conclusion,

patients with active pulmonary TB have low circulating granulysin but high IFN-γ concentrations before treatment indicating their possible role in controlling M. tuberculosis infection. We wish to thank the staff of the TB/HIV Research Project, a collaborative research

project of the Research Institute of Tuberculosis (RIT); Japan Anti-Tuberculosis Association (JATA) and Ministry of Public Health of Thailand, for blood collection and provision of clinical ID-8 data. We thank the patients for their kind participation in the study. This study was supported by the Royal Golden Jubilee Ph.D. Program of the Thailand Research Fund (Grant No. PHD/0227/2549), Faculty of Tropical Medicine, Mahidol University, an Intramural Grant from the Department of Medical Science, Ministry of Public Health, Thailand, a Health and Labor Science Grant from Ministry of Health, Labor and Welfare, Japan and a International Collaborative Study Grant from the Human Science Foundation, Japan. “
“The pattern of immune response to a vaccine antigen can influence both efficacy and adverse events. Th2-cell-deviated responses have been implicated in both human and murine susceptibility to enhanced disease following formalin-inactivated (FI) vaccines for measles and RSV. In this study, we used the Th2-cell-deviated murine model of FI-RSV vaccination to test the ability of a dominant negative, cell-penetrating peptide inhibitor of STAT6 (STAT6 inhibitory peptide (IP)) to modulate the vaccine-induced predisposition to exaggerated inflammation during later RSV infection.