Latent Mycobacterium tuberculosis Infection Is Associated With a Higher Frequency of Mucosal-Associated Invariant T and Invariant Natural Killer T Cells.

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorPAQUIN-PROULX, Dominic
dc.contributor.authorCOSTA, Priscilla R.
dc.contributor.authorSILVEIRA, Cassia G. Terrassani
dc.contributor.authorMARMORATO, Mariana P.
dc.contributor.authorCERQUEIRA, Natalia B.
dc.contributor.authorSUTTON, Matthew S.
dc.contributor.authorO'CONNOR, Shelby L.
dc.contributor.authorCARVALHO, Karina I.
dc.contributor.authorNIXON, Douglas F.
dc.contributor.authorKALLAS, Esper G.
dc.date.accessioned2018-09-13T15:22:30Z
dc.date.available2018-09-13T15:22:30Z
dc.date.issued2018
dc.description.abstractIncreasing drug resistance and the lack of an effective vaccine are the main factors contributing to Mycobacterium tuberculosis (Mtb) being a major cause of death globally. Despite intensive research efforts, it is not well understood why some individuals control Mtb infection and some others develop active disease. HIV-1 infection is associated with an increased incidence of active tuberculosis, even in virally suppressed individuals. Mucosal-associated invariant T (MAIT) and invariant natural killer T (iNKT) cells are innate T cells that can recognize Mtb-infected cells. Contradicting results regarding the frequency of MAIT cells in latent Mtb infection have been reported. In this confirmatory study, we investigated the frequency, phenotype, and IFN gamma production of MAIT and iNKT cells in subjects with latent or active Mtb infection. We found that the frequency of both cell types was increased in subjects with latent Mtb infection compared with uninfected individuals or subjects with active infection. We found no change in the expression of HLA-DR, PD-1, and CCR6, as well as the production of IFN. by MAIT and iNKT cells, among subjects with latent Mtb infection or uninfected controls. The proportion of CD4-CD8+ MAIT cells in individuals with latent Mtb infection was, however, increased. HIV-1 infection was associated with a loss of MAIT and iNKT cells, and the residual cells had elevated expression of the exhaustion marker PD-1. Altogether, the results suggest a role for MAIT and iNKT cells in immunity against Mtb and show a deleterious impact of HIV-1 infection on those cells.
dc.description.indexPubMed
dc.description.sponsorshipNIAID [R01 AI52731]
dc.description.sponsorship[R21 AI127127]
dc.identifier.citationFRONTIERS IN IMMUNOLOGY, v.9, article ID 1394, 9p, 2018
dc.identifier.doi10.3389/fimmu.2018.01394
dc.identifier.issn1664-3224
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/27987
dc.language.isoeng
dc.publisherFRONTIERS MEDIA SA
dc.relation.ispartofFrontiers in Immunology
dc.rightsopenAccess
dc.rights.holderCopyright FRONTIERS MEDIA SA
dc.subjectmucosal-associated invariant T cells
dc.subjectinvariant natural killer T cells
dc.subjectMycobacterium tuberculosis
dc.subjectHIV-1
dc.subjectCCR6
dc.subject.othercd1d-restricted nkt cells
dc.subject.otherantiretroviral therapy
dc.subject.otherhiv-1 infection
dc.subject.othermait cells
dc.subject.otheractivation
dc.subject.otherheterogeneity
dc.subject.otherindividuals
dc.subject.othermetabolites
dc.subject.otherresponses
dc.subject.othercd4(+)
dc.subject.wosImmunology
dc.titleLatent Mycobacterium tuberculosis Infection Is Associated With a Higher Frequency of Mucosal-Associated Invariant T and Invariant Natural Killer T Cells.
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.affiliation.countryEstados Unidos
hcfmusp.affiliation.countryisous
hcfmusp.author.externalPAQUIN-PROULX, Dominic:George Washington Univ, Dept Microbiol Immunol & Trop Med, Washington, DC 20052 USA
hcfmusp.author.externalSUTTON, Matthew S.:Univ Wisconsin, Dept Pathol & Lab Med, Madison, WI USA
hcfmusp.author.externalO'CONNOR, Shelby L.:Univ Wisconsin, Dept Pathol & Lab Med, Madison, WI USA
hcfmusp.author.externalCARVALHO, Karina I.:Hosp Israelita Albert Einstein, Inst Israelita Ensino & Pesquisa, Sao Paulo, Brazil
hcfmusp.author.externalNIXON, Douglas F.:George Washington Univ, Dept Microbiol Immunol & Trop Med, Washington, DC 20052 USA
hcfmusp.citation.scopus31
hcfmusp.contributor.author-fmusphcPRISCILLA RAMOS COSTA
hcfmusp.contributor.author-fmusphcCASSIA GISELE TERRASSANI SILVEIRA
hcfmusp.contributor.author-fmusphcMARIANA PRADO MARMORATO
hcfmusp.contributor.author-fmusphcNATALIA BARROS CERQUEIRA
hcfmusp.contributor.author-fmusphcESPER GEORGES KALLAS
hcfmusp.description.articlenumber1394
hcfmusp.description.volume9
hcfmusp.origemWOS
hcfmusp.origem.pubmed29971068
hcfmusp.origem.scopus2-s2.0-85048652588
hcfmusp.origem.wosWOS:000435723800001
hcfmusp.publisher.cityLAUSANNE
hcfmusp.publisher.countrySWITZERLAND
hcfmusp.relation.referenceAzakami K, 2009, BLOOD, V114, P3208, DOI 10.1182/blood-2009-02-203042
hcfmusp.relation.referenceCanaday DH, 2001, J IMMUNOL, V167, P2734, DOI 10.4049/jimmunol.167.5.2734
hcfmusp.relation.referenceChancellor A, 2017, TUBERCULOSIS, V105, P86, DOI 10.1016/j.tube.2017.04.011
hcfmusp.relation.referenceCorbett AJ, 2014, NATURE, V509, P361, DOI 10.1038/nature13160
hcfmusp.relation.referenceCosgrove C, 2013, BLOOD, V121, P951, DOI 10.1182/blood-2012-06-436436
hcfmusp.relation.referenceDias J, 2017, P NATL ACAD SCI USA, V114, pE5434, DOI 10.1073/pnas.1705759114
hcfmusp.relation.referenceDias J, 2016, J LEUKOCYTE BIOL, V100, P233, DOI 10.1189/jlb.4TA0815-391RR
hcfmusp.relation.referenceFLYNN JL, 1993, J EXP MED, V178, P2249, DOI 10.1084/jem.178.6.2249
hcfmusp.relation.referenceGandhi NR, 2006, LANCET, V368, P1575, DOI 10.1016/S0140-6736(06)69573-1
hcfmusp.relation.referenceGherardin NA, 2018, IMMUNOL CELL BIOL, V96, P507, DOI 10.1111/imcb.12021
hcfmusp.relation.referenceGold MC, 2010, PLOS BIOL, V8, DOI 10.1371/journal.pbio.1000407
hcfmusp.relation.referenceGreene JM, 2017, MUCOSAL IMMUNOL, V10, P802, DOI 10.1038/mi.2016.91
hcfmusp.relation.referenceGupta A, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0034156
hcfmusp.relation.referenceHuang SX, 2016, FRONT IMMUNOL, V7, DOI 10.3389/fimmu.2016.00594
hcfmusp.relation.referenceHuang SX, 2009, P NATL ACAD SCI USA, V106, P8290, DOI 10.1073/pnas.0903196106
hcfmusp.relation.referenceJiang J, 2016, SCI REP-UK, V6, DOI 10.1038/srep32320
hcfmusp.relation.referenceKee SJ, 2012, INFECT IMMUN, V80, P2100, DOI 10.1128/IAI.06018-11
hcfmusp.relation.referenceKinjo Y, 2005, NATURE, V434, P520, DOI 10.1038/nature03407
hcfmusp.relation.referenceKjer-Nielsen L, 2012, NATURE, V491, P717, DOI 10.1038/nature11605
hcfmusp.relation.referenceKurioka A, 2017, FRONT IMMUNOL, V8, DOI [10.3389/fimmu.2017.0103, 10.3389/fimmu.2017.01031]
hcfmusp.relation.referenceKwon YS, 2015, TUBERCULOSIS, V95, P267, DOI 10.1016/j.tube.2015.03.004
hcfmusp.relation.referenceLawn SD, 2011, LANCET, V378, P57, DOI 10.1016/S0140-6736(10)62173-3
hcfmusp.relation.referenceLawn SD, 2009, AIDS, V23, P1717, DOI 10.1097/QAD.0b013e32832d3b6d
hcfmusp.relation.referenceLe Bourhis L, 2010, NAT IMMUNOL, V11, P701, DOI 10.1038/ni.1890
hcfmusp.relation.referenceLeeansyah E, 2013, BLOOD, V121, P1124, DOI 10.1182/blood-2012-07-445429
hcfmusp.relation.referenceMangtani P, 2014, CLIN INFECT DIS, V58, P470, DOI 10.1093/cid/cit790
hcfmusp.relation.referenceMarinho J, 2005, JAIDS-J ACQ IMM DEF, V40, P625, DOI 10.1097/01.qai.0000174252.73516.7a
hcfmusp.relation.referenceMattner J, 2005, NATURE, V434, P525, DOI 10.1038/nature03408
hcfmusp.relation.referenceMoll M, 2006, BLOOD, V107, P3081, DOI 10.1182/blood-2005-09-3636
hcfmusp.relation.referenceMontoya CJ, 2008, CLIN IMMUNOL, V127, P1, DOI 10.1016/j.clim.2007.12.006
hcfmusp.relation.referenceMotsinger A, 2002, J EXP MED, V195, P869, DOI 10.1084/jem.20011712
hcfmusp.relation.referencePaquin-Proulx D, 2017, MUCOSAL IMMUNOL, V10, P69, DOI 10.1038/mi.2016.34
hcfmusp.relation.referencePaquin-Proulx D, 2017, PLOS ONE, V12, DOI 10.1371/journal.pone.0175345
hcfmusp.relation.referenceGrassi MFR, 2016, BMC INFECT DIS, V16, DOI 10.1186/s12879-016-1428-z
hcfmusp.relation.referenceSada-Ovalle I, 2008, PLOS PATHOG, V4, DOI 10.1371/journal.ppat.1000239
hcfmusp.relation.referenceSaeidi A, 2015, PLOS ONE, V10, DOI 10.1371/journal.pone.0124659
hcfmusp.relation.referenceSakai S, 2016, PLOS PATHOG, V12, DOI 10.1371/journal.ppat.1005667
hcfmusp.relation.referenceSakala IG, 2015, J IMMUNOL, V195, P587, DOI 10.4049/jimmunol.1402545
hcfmusp.relation.referenceSerbina NV, 2001, J IMMUNOL, V167, P6991, DOI 10.4049/jimmunol.167.12.6991
hcfmusp.relation.referenceSnyder-Cappione JE, 2007, J INFECT DIS, V195, P1361, DOI 10.1086/513567
hcfmusp.relation.referenceSortino O, 2018, AIDS, V32, P825, DOI [10.1097/QAD.0000000000001760, 10.1097/qad.0000000000001760]
hcfmusp.relation.referenceWong EB, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0083474
hcfmusp.relation.referenceYang QT, 2015, SCI REP-UK, V5, DOI 10.1038/srep17918
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