Mycobacterium tuberculosislpdC, Rv0462, induces dendritic cell maturation and Th1 polarization |
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| Authors: | Heo Deok Rim Shin Sung Jae Kim Woo Sik Noh Kyung Tae Park Jin Wook Son Kwang Hee Park Won Sun Lee Min-Goo Kim Daejin Shin Yong Kyoo Jung In Duk Park Yeong-Min |
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| Institution: | aDepartment of Microbiology and Immunology, School of Medicine, Pusan National University, Beom-eo Ri, Mulgum Eop, Yangsan, Gyeongsangnam-do 626-770, South Korea;bDepartment of Microbiology, College of Medicine, Chungnam National University, Munwha-Dong, Jung-Ku, Daejeon 301-747, South Korea;cDepartment of Physiology, Kangwon National University, School of Medicine, Chuncheon 200-701, South Korea;dDepartment of Physiology, Korea University, College of Medicine, Anam-dong, Sungbuk-Gu, Seoul 136-705, South Korea;eDepartment of Anatomy, Chung-Ang University, College of Medicine, 221 Heuksuk-Dong, Dongjak-Ku, Seoul 156-756, South Korea;fDepartment of Pharmacology, Chung-Ang University, College of Medicine, 221 Heuksuk-Dong, Dongjak-Ku, Seoul 156-756, South Korea;gResearch Institute of Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Beom-eo Ri, Mulgum Eop, Yangsan, Gyeongsangnam-do 626-770, South Korea |
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| Abstract: | 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. |
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| Keywords: | Dendritic cells Th1 polarization MAPKs Mycobacterium tuberculosis Rv0462 |
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