Mycobacterium tuberculosis lpdC, Rv0462, induces dendritic cell maturation and Th1 polarization
- 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
- Issue Date
- 5-8월-2011
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Dendritic cells; Th1 polarization; MAPKs; Mycobacterium tuberculosis; Rv0462
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.411, no.3, pp.642 - 647
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 411
- Number
- 3
- Start Page
- 642
- End Page
- 647
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/111807
- DOI
- 10.1016/j.bbrc.2011.07.013
- ISSN
- 0006-291X
- 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, Ry0462, induce maturation and activation of DCs involved in the MAPKs signaling pathway. Moreover, Rv0462-treated DCs activated naive T cells, polarized CD4(+) and CD8(+) T cells to secrete IFN-gamma 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. Crown Copyright (C) 2011 Published by Elsevier Inc. All rights reserved.
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