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Mycobacterium tuberculosis RpfB drives Th1-type T cell immunity via a TLR4-dependent activation of dendritic cells

DC Field Value Language
dc.contributor.author김종석-
dc.contributor.author신성재-
dc.contributor.author이기훈-
dc.contributor.author장병기-
dc.contributor.author조상래-
dc.date.accessioned2014-12-18T09:15:47Z-
dc.date.available2014-12-18T09:15:47Z-
dc.date.issued2013-
dc.identifier.issn0741-5400-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/87840-
dc.description.abstractThe failure of Mycobacterium bovis BCG as a TB vaccine against TB reactivation suggests that latency-associated proteins should be included in alternative TB vaccine development. Further, antigens known to generate protective immunity against the strong Th1 stimulatory response to reactivated TB should be included in novel vaccine design. Recent studies have emphasized the importance of Rpfs from Mycobacterium tuberculosis in the reactivation process and cellular immunity. However, little is known about how RpfB mediates protective immunity against M. tuberculosis. Here, we investigated the functional roles and signaling mechanisms of RpfB in DCs and its implications in the development of T cell immunity. DCs treated with RpfB displayed features of mature and functional status, with elevated expression of cell surface molecules (CD80, CD86, and MHC class I and II) and proinflammatory cytokine production (TNF-α, IL-1β, IL-6, and IL-12p70). Activation of DCs was mediated by direct binding of RpfB to TLR4, followed by MyD88/TRIF-dependent signaling to MAPKs and NF-κB signaling pathways. Specifically, we found that the RpfB G5 domain is the most important part in RpfB binding to TLR4. RpfB-treated DCs effectively polarized naïve CD4(+) and CD8(+) T cells to secrete IFN-γ and IL-2. Importantly, RpfB induced the expansion of memory CD4(+)/CD8(+)CD44(high)CD62L(low) T cells in the spleen of M. tuberculosis-infected mice. Our data suggest that RpfB regulates innate immunity and activates adaptive immunity through TLR4, a finding that may help in the design of more effective vaccines.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfJOURNAL OF LEUKOCYTE BIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHBacterial Proteins/metabolism*-
dc.subject.MESHCD4-Positive T-Lymphocytes/cytology-
dc.subject.MESHCD4-Positive T-Lymphocytes/metabolism-
dc.subject.MESHCD8-Positive T-Lymphocytes/cytology-
dc.subject.MESHCD8-Positive T-Lymphocytes/metabolism-
dc.subject.MESHCell Death-
dc.subject.MESHCell Differentiation/immunology-
dc.subject.MESHCytokines/metabolism-
dc.subject.MESHDendritic Cells/cytology-
dc.subject.MESHDendritic Cells/immunology*-
dc.subject.MESHEndotoxins/metabolism-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHFemale-
dc.subject.MESHImmunity, Cellular/immunology*-
dc.subject.MESHImmunologic Memory-
dc.subject.MESHMice-
dc.subject.MESHMitogen-Activated Protein Kinases/metabolism-
dc.subject.MESHMycobacterium tuberculosis/immunology*-
dc.subject.MESHNF-kappa B/metabolism-
dc.subject.MESHNeutralization Tests-
dc.subject.MESHPhenotype-
dc.subject.MESHProtein Binding-
dc.subject.MESHReproducibility of Results-
dc.subject.MESHSequence Deletion/genetics-
dc.subject.MESHSignal Transduction/immunology-
dc.subject.MESHTh1 Cells/cytology-
dc.subject.MESHTh1 Cells/immunology*-
dc.subject.MESHToll-Like Receptor 2/metabolism-
dc.subject.MESHToll-Like Receptor 4/metabolism*-
dc.titleMycobacterium tuberculosis RpfB drives Th1-type T cell immunity via a TLR4-dependent activation of dendritic cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Microbiology (미생물학)-
dc.contributor.googleauthorJong-Seok Kim-
dc.contributor.googleauthorWoo Sik Kim-
dc.contributor.googleauthorHan-Gyu Choi-
dc.contributor.googleauthorByungki Jang-
dc.contributor.googleauthorKeehoon Lee-
dc.contributor.googleauthorJong-Hwan Park-
dc.contributor.googleauthorHwa-Jung Kim-
dc.contributor.googleauthorSang-Nae Cho-
dc.contributor.googleauthorSung Jae Shin-
dc.identifier.doi10.1189/jlb.0912435-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02699-
dc.contributor.localIdA03429-
dc.contributor.localIdA03824-
dc.contributor.localIdA00920-
dc.contributor.localIdA02114-
dc.relation.journalcodeJ01559-
dc.identifier.eissn1938-3673-
dc.identifier.pmid23825389-
dc.identifier.urlhttp://www.jleukbio.org/content/94/4/733.long-
dc.subject.keywordGATA-3-
dc.subject.keywordT-bet-
dc.subject.keywordVaccine-
dc.contributor.alternativeNameKim, Jong Seok-
dc.contributor.alternativeNameShin, Sung Jae-
dc.contributor.alternativeNameLee, Kee Hoon-
dc.contributor.alternativeNameJang, Byung Ki-
dc.contributor.alternativeNameCho, Sang Nae-
dc.contributor.affiliatedAuthorLee, Kee Hoon-
dc.contributor.affiliatedAuthorJang, Byung Ki-
dc.contributor.affiliatedAuthorCho, Sang Nae-
dc.contributor.affiliatedAuthorKim, Jong Seok-
dc.contributor.affiliatedAuthorShin, Sung Jae-
dc.rights.accessRightsnot free-
dc.citation.volume94-
dc.citation.number4-
dc.citation.startPage733-
dc.citation.endPage749-
dc.identifier.bibliographicCitationJOURNAL OF LEUKOCYTE BIOLOGY, Vol.94(4) : 733-749, 2013-
dc.identifier.rimsid32555-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers

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