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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2019.4
- 수록면
- 56 - 65 (10page)
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6-kDa early secretory antigenic target (ESAT6), a virulent factor of Mycobacterium tuberculosis, is involved in immune regulation. However, the underlying mechanism behind the activation and maturation of dendritic cells (DCs) by ESAT6 remains unclear. In this study, we investigated the effect on TLRs signaling on the regulation of ESAT6-induced activation and maturation of DCs. ESAT6 induced production of IL-6, TNF-α, and IL-12p40 in bone marrowderived dendritic cells (BMDCs) from wild-type and TLR2-deficient mice, with this induction abolished in TLR4-deficient cells. NF-κB is essential for the ESAT6-induced production of the cytokines in BMDCs. TLR4 was also required for ESAT6-induced activation of NF-κB and MAPKs in BMDCs. ESAT6 additionally upregulated the expression of surface molecules CD80, CD86, and MHC-II, and also promoted the ability of CD4+ T cells to secrete IFN-γ via the TLR4-dependent pathway. Our findings suggest that TLR4 is critical in the activation and maturation of DCs in response to ESAT6.
목차
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS AND DISCUSSION
REFERENCES
참고문헌 (29)
참고문헌 신청
Pai M / 2016 / Tuberculosis / Nat Rev Dis Primers 2:16076
World Health Organization / 2017 / Global Tuberculosis Report 2017
Wong KW / 2017 / The role of ESX-1 in Mycobacterium tuberculosis pathogenesis / Microbiol Spectr 5
Gröschel MI / 2016 / ESX secretion systems: mycobacterial evolution to counter host immunity / Nat Rev Microbiol 14:677~691
Janssens S / 2003 / Role of Toll-like receptors in pathogen recognition / Clin Microbiol Rev 16:637~646
World Health Organization / 2017 / Global Tuberculosis Report 2017
Wong KW / 2017 / The role of ESX-1 in Mycobacterium tuberculosis pathogenesis / Microbiol Spectr 5
Gröschel MI / 2016 / ESX secretion systems: mycobacterial evolution to counter host immunity / Nat Rev Microbiol 14:677~691
Janssens S / 2003 / Role of Toll-like receptors in pathogen recognition / Clin Microbiol Rev 16:637~646
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UCI(KEPA) : I410-ECN-0101-2019-517-000788719