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dc.contributor.author
Wang, Xisheng
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Barnes, Peter F.
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Huang, Fangfang
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Alvarez, Ivana Belén
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Neuenschwander, Pierre F.
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Sherman, David R.
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Samten, Buka
dc.date.available
2017-05-04T20:29:57Z
dc.date.issued
2012-09
dc.identifier.citation
Wang, Xisheng; Barnes, Peter F.; Huang, Fangfang; Alvarez, Ivana Belén; Neuenschwander, Pierre F.; et al.; Early secreted antigenic target of 6-kDa protein of Mycobacterium tuberculosis primes dendritic cells to stimulate Th17 and inhibit Th1 immune responses; Amer Assoc Immunologists; Journal Of Immunology; 189; 6; 9-2012; 3092-3103
dc.identifier.issn
0022-1767
dc.identifier.uri
http://hdl.handle.net/11336/15999
dc.description.abstract
Early secreted antigenic target of 6 kDa (ESAT-6) of Mycobacterium tuberculosis is a T cell Ag that is a potential vaccine candidate, but it is also a virulence factor that mediates pathogenicity. To better understand the effects of ESAT-6 on the immune response, we studied the effect of ESAT-6 on human dendritic cells (DCs). Peripheral blood monocytes were treated with GM-CSF and IL-4 to yield immature DCs, which were matured by addition of LPS and CD40 ligand (CD40L), with or without ESAT-6. ESAT-6 inhibited LPS/CD40L-induced DC expression of costimulatory molecules, reduced DC-stimulated allogeneic T cell proliferation and IL-2 and IFN-γ production, and enhanced IL-17 production. ESAT-6-treated DCs also increased IL-17 and reduced IFN-γ production by M. tuberculosis-specific autologous T cells. ESAT-6 inhibited LPS/CD40L-induced DC production of IL-12 and enhanced that of IL-23 and IL-1β, without affecting secretion of TNF-α, IL-6, or IL-8 through specific interaction with immature DCs. The effects of ESAT-6 were not mediated through cAMP or p38 MAPK. Medium from ESAT-6-conditioned DCs increased IL-17 and reduced IFN-γ production by T cells stimulated with anti-CD3 plus anti-CD28, and ESAT-6-induced IL-17 production was blocked by neutralizing both IL-23 and IL-1β. ESAT-6 reduced LPS/CD40L-stimulated transcription of IL-12p35 and enhanced that of IL-23p19 through inhibition of IFN regulatory factor-1 and upregulation of activating transcription factor-2 and c-Jun, transcriptional regulators of IL-12p35 and IL-23p19, respectively. We conclude that ESAT-6 increases DC production of IL-23 and IL-1β while inhibiting that of IL-12, thus enhancing Th17 at the expense of protective Th1 responses.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Amer Assoc Immunologists
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Tuberculosis
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Esat-6
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Cytokines
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Otras Ciencias Biológicas
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Early secreted antigenic target of 6-kDa protein of Mycobacterium tuberculosis primes dendritic cells to stimulate Th17 and inhibit Th1 immune responses
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2017-05-03T19:43:00Z
dc.identifier.eissn
1550-6606
dc.journal.volume
189
dc.journal.number
6
dc.journal.pagination
3092-3103
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Bethesda
dc.description.fil
Fil: Wang, Xisheng. University of Texas Health Science Center; Estados Unidos
dc.description.fil
Fil: Barnes, Peter F.. University of Texas Health Science Center; Estados Unidos
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Fil: Huang, Fangfang. University of Texas Health Science Center; Estados Unidos
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Fil: Alvarez, Ivana Belén. University of Texas Health Science Center; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
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Fil: Neuenschwander, Pierre F.. University of Texas Health Science Center; Estados Unidos
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Fil: Sherman, David R.. University of Washington; Estados Unidos. Seattle Biomedical Research Institute; Estados Unidos
dc.description.fil
Fil: Samten, Buka. University of Texas Health Science Center; Estados Unidos
dc.journal.title
Journal Of Immunology
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.4049/jimmunol.1200573
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.jimmunol.org/content/189/6/3092
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