Chung YT, et al. - Researchers here aimed at examining the role of cAMP in the immune response to Mycobacterium tuberculosis (Mtb) infection by performing determination of cAMP levels in peripheral blood mononuclear cells (PBMC) from tuberculosis patients and the mechanisms for cAMP suppression of T cell IFN-γ production. Mtb-induced IFN-γ production by PBMC was inhibited by cAMP analogs in a PKA type I, but not PKA type II or EPAC (early exchange protein directly activated by cAMP) dependent manner. PKA type I specific cAMP analogs significantly reduced Mtb-induced IFN-γ promoter binding activities and expression of CREB, ATF-2, and c-Jun as determined by gel shift assay and western blotting, respectively. Findings thereby suggested that increased cAMP inhibited T-cell IFN-γ production through PKA type I pathway.