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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Arquivos
art_PAQUIN-PROULX_Latent_Mycobacterium_tuberculosis_Infection_Is_Associated_With_a_2018.PDF (2.49 MB)
Citações na Scopus
31
Tipo de produção
article
Data de publicação
2018
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
FRONTIERS MEDIA SA
Autores
PAQUIN-PROULX, Dominic
SUTTON, Matthew S.
O'CONNOR, Shelby L.
CARVALHO, Karina I.
NIXON, Douglas F.
Citação
FRONTIERS IN IMMUNOLOGY, v.9, article ID 1394, 9p, 2018
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Increasing 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.
Palavras-chave
mucosal-associated invariant T cells, invariant natural killer T cells, Mycobacterium tuberculosis, HIV-1, CCR6
URI
https://observatorio.fm.usp.br/handle/OPI/27987
Referências
  1. Azakami K, 2009, BLOOD, V114, P3208, DOI 10.1182/blood-2009-02-203042
  2. Canaday DH, 2001, J IMMUNOL, V167, P2734, DOI 10.4049/jimmunol.167.5.2734
  3. Chancellor A, 2017, TUBERCULOSIS, V105, P86, DOI 10.1016/j.tube.2017.04.011
  4. Corbett AJ, 2014, NATURE, V509, P361, DOI 10.1038/nature13160
  5. Cosgrove C, 2013, BLOOD, V121, P951, DOI 10.1182/blood-2012-06-436436
  6. Dias J, 2017, P NATL ACAD SCI USA, V114, pE5434, DOI 10.1073/pnas.1705759114
  7. Dias J, 2016, J LEUKOCYTE BIOL, V100, P233, DOI 10.1189/jlb.4TA0815-391RR
  8. FLYNN JL, 1993, J EXP MED, V178, P2249, DOI 10.1084/jem.178.6.2249
  9. Gandhi NR, 2006, LANCET, V368, P1575, DOI 10.1016/S0140-6736(06)69573-1
  10. Gherardin NA, 2018, IMMUNOL CELL BIOL, V96, P507, DOI 10.1111/imcb.12021
  11. Gold MC, 2010, PLOS BIOL, V8, DOI 10.1371/journal.pbio.1000407
  12. Greene JM, 2017, MUCOSAL IMMUNOL, V10, P802, DOI 10.1038/mi.2016.91
  13. Gupta A, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0034156
  14. Huang SX, 2016, FRONT IMMUNOL, V7, DOI 10.3389/fimmu.2016.00594
  15. Huang SX, 2009, P NATL ACAD SCI USA, V106, P8290, DOI 10.1073/pnas.0903196106
  16. Jiang J, 2016, SCI REP-UK, V6, DOI 10.1038/srep32320
  17. Kee SJ, 2012, INFECT IMMUN, V80, P2100, DOI 10.1128/IAI.06018-11
  18. Kinjo Y, 2005, NATURE, V434, P520, DOI 10.1038/nature03407
  19. Kjer-Nielsen L, 2012, NATURE, V491, P717, DOI 10.1038/nature11605
  20. Kurioka A, 2017, FRONT IMMUNOL, V8, DOI [10.3389/fimmu.2017.0103, 10.3389/fimmu.2017.01031]
  21. Kwon YS, 2015, TUBERCULOSIS, V95, P267, DOI 10.1016/j.tube.2015.03.004
  22. Lawn SD, 2011, LANCET, V378, P57, DOI 10.1016/S0140-6736(10)62173-3
  23. Lawn SD, 2009, AIDS, V23, P1717, DOI 10.1097/QAD.0b013e32832d3b6d
  24. Le Bourhis L, 2010, NAT IMMUNOL, V11, P701, DOI 10.1038/ni.1890
  25. Leeansyah E, 2013, BLOOD, V121, P1124, DOI 10.1182/blood-2012-07-445429
  26. Mangtani P, 2014, CLIN INFECT DIS, V58, P470, DOI 10.1093/cid/cit790
  27. Marinho J, 2005, JAIDS-J ACQ IMM DEF, V40, P625, DOI 10.1097/01.qai.0000174252.73516.7a
  28. Mattner J, 2005, NATURE, V434, P525, DOI 10.1038/nature03408
  29. Moll M, 2006, BLOOD, V107, P3081, DOI 10.1182/blood-2005-09-3636
  30. Montoya CJ, 2008, CLIN IMMUNOL, V127, P1, DOI 10.1016/j.clim.2007.12.006
  31. Motsinger A, 2002, J EXP MED, V195, P869, DOI 10.1084/jem.20011712
  32. Paquin-Proulx D, 2017, MUCOSAL IMMUNOL, V10, P69, DOI 10.1038/mi.2016.34
  33. Paquin-Proulx D, 2017, PLOS ONE, V12, DOI 10.1371/journal.pone.0175345
  34. Grassi MFR, 2016, BMC INFECT DIS, V16, DOI 10.1186/s12879-016-1428-z
  35. Sada-Ovalle I, 2008, PLOS PATHOG, V4, DOI 10.1371/journal.ppat.1000239
  36. Saeidi A, 2015, PLOS ONE, V10, DOI 10.1371/journal.pone.0124659
  37. Sakai S, 2016, PLOS PATHOG, V12, DOI 10.1371/journal.ppat.1005667
  38. Sakala IG, 2015, J IMMUNOL, V195, P587, DOI 10.4049/jimmunol.1402545
  39. Serbina NV, 2001, J IMMUNOL, V167, P6991, DOI 10.4049/jimmunol.167.12.6991
  40. Snyder-Cappione JE, 2007, J INFECT DIS, V195, P1361, DOI 10.1086/513567
  41. Sortino O, 2018, AIDS, V32, P825, DOI [10.1097/QAD.0000000000001760, 10.1097/qad.0000000000001760]
  42. Wong EB, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0083474
  43. Yang QT, 2015, SCI REP-UK, V5, DOI 10.1038/srep17918

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - FM/MIP
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - LIM/60
Artigos e Materiais de Revistas Científicas - ODS/03