Department of Microbiology and Immunology, School of Medicine, Pusan National University, Beom-eo Ri, Mulgum Eop, Yangsan, Gyeongsangnam-do 626-770, South Korea.
Biochem Biophys Res Commun. 2011 Aug 5;411(3):642-7. doi: 10.1016/j.bbrc.2011.07.013. Epub 2011 Jul 18.
Mycobacterium tuberculosis, the etiological factor of pulmonary tuberculosis, causes significant morbidity and mortality worldwide. Activation of host immune responses for containment of mycobacterial infections involves participation of innate immune cells, such as dendritic cells (DCs). In this study, we demonstrated that the gene encoding lipoamide dehydrogenase C (lpdC) from M. tuberculosis, Rv0462, induce maturation and activation of DCs involved in the MAPKs signaling pathway. Moreover, Rv0462-treated DCs activated naïve T cells, polarized CD4(+) and CD8(+) T cells to secrete IFN-γ in syngeneic mixed lymphocyte reactions, which would be expected to contribute to Th1 polarization of the immune response. Our results suggest that Rv0462 can contribute to the innate and adaptive immune responses during tuberculosis infection, and thus modulate the clinical course of tuberculosis.
结核分枝杆菌是肺结核的病因，在全球范围内造成了重大的发病率和死亡率。宿主免疫反应的激活对于控制分枝杆菌感染涉及固有免疫细胞的参与，如树突状细胞（DCs）。在这项研究中，我们证明了来自结核分枝杆菌的编码脂酰脱氢酶 C（lpdC）的基因，Rv0462，诱导参与 MAPKs 信号通路的 DC 的成熟和激活。此外，Rv0462 处理的 DCs 激活了幼稚 T 细胞，极化 CD4(+)和 CD8(+)T 细胞在同基因混合淋巴细胞反应中分泌 IFN-γ，这有望促进免疫反应的 Th1 极化。我们的结果表明，Rv0462 可以在结核感染期间有助于固有和适应性免疫反应，从而调节结核的临床病程。
