Th9 cytokines response and its possible implications in the immunopathogenesis of leprosy

Carregando...
Imagem de Miniatura
Citações na Scopus
19
Tipo de produção
article
Data de publicação
2017
Editora
BMJ PUBLISHING GROUP
Indexadores
Título da Revista
ISSN da Revista
Título do Volume
Autores
SOUSA, Jorge Rodrigues de
ALMEIDA, Dandara Simone Maia de
BARROS, Luiz Fernando Lima
CARNEIRO, Francisca Regina Oliveira
DIAS JR., Leonidas Braga
AARAO, Tinara Leila de Souza
QUARESMA, Juarez Antonio Simoes
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
JOURNAL OF CLINICAL PATHOLOGY, v.70, n.6, p.521-527, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Aims Leprosy is an infectious-contagious disease whose clinical evolution depends on the interaction of the infectious agent with the immune response of the host, leading to a clinical spectrum that ranges from lepromatous leprosy (susceptibility, LL) to tuberculoid leprosy (resistance, TT). The immune response profile will depend on the pattern of cytokine production and on the activity of macrophages during infection. Classically, the clinical evolution of leprosy has been associated with Th1/Th2 cytokine profiles, but the role of new cytokine profiles such as T helper 9 (Th9) remains to be elucidated. Methods To evaluate the tissue expression profile of these cytokines, a cross-sectional study was conducted using a sample of 30 leprosy skin lesion biopsies obtained from patients with leprosy, 16 TT and 14 lepromatous LL. Results Immunohistochemical analysis revealed a significant difference in interleukin (IL)-9, IL-4 transforming growth factor (TGF)-beta and IL-10 levels between the two groups. IL-9 was more expressed in TT lesions compared with LL lesions. Higher expression of IL-4, IL-10 and TGF-beta was observed in LL compared with TT. IL-4, IL-10 and TGF-beta tended to be negatively correlated with the expression of IL-9, indicating a possible antagonistic activity in tissue. Conclusions The results suggest that Th9 lymphocytes may be involved in the response to Mycobacterium leprae, positively or negatively regulating microbicidal activity of the local immune system in the disease.
Palavras-chave
Referências
  1. Aarao Tinara Leila de Sousa, 2016, Microb Pathog, V90, P64, DOI 10.1016/j.micpath.2015.11.019
  2. Alexander J, 2012, FRONT IMMUNOL, V3, DOI 10.3389/fimmu.2012.00080
  3. Alvarez I, 2013, J IMMUNOL S, V190
  4. Anuradha R, 2016, PLOS NEGLECT TROP D, V10, DOI 10.1371/journal.pntd.0004317
  5. Callegaro D, 2010, J DRUGS DERMATOL, V9, P1373
  6. Cardoso CC, 2011, FUTURE MICROBIOL, V6, P533, DOI [10.2217/fmb.11.39, 10.2217/FMB.11.39]
  7. Chakrabarti Srabani, 2016, Iran J Pathol, V11, P54
  8. Chang HC, 2010, NAT IMMUNOL, V11, P527, DOI 10.1038/ni.1867
  9. Dantas AT, 2015, DIS MARKERS, V2015
  10. Dardalhon V, 2008, NAT IMMUNOL, V9, P1347, DOI 10.1038/ni.1677
  11. da Silva MV, 2015, J IMMUNOL RES, V2015
  12. de Sousa JR, 2016, ACTA TROP, V157, P108, DOI 10.1016/j.actatropica.2016.01.008
  13. De Oliveira FT, 2014, INFECT IMMUN, V82, P3968, DOI 10.1128/IAI.02194-14
  14. Fang YJ, 2015, J SURG ONCOL, V111, P969, DOI 10.1002/jso.23930
  15. Finiasz MR, 2007, CLIN EXP IMMUNOL, V147, P139, DOI 10.1111/j.1365-2249.2006.03241.x
  16. Rojas-Zuleta WG, 2016, AUTOIMMUN REV, V15, P649, DOI 10.1016/j.autrev.2016.02.020
  17. Golubovskaya V, 2016, CANCERS, V8, DOI 10.3390/cancers8030036
  18. Gomez-Rodriguez J, 2016, NAT COMMUN, V7, DOI 10.1038/ncomms10857
  19. Goswami R, 2011, J IMMUNOL, V186, P3283, DOI 10.4049/jimmunol.1003049
  20. Harris J, 2007, IMMUNITY, V27, P505, DOI 10.1016/j.immuni.2007.07.022
  21. Hirahara K, 2016, INT IMMUNOL, V28, P163, DOI 10.1093/intimm/dxw006
  22. Kaplan MH, 2015, NAT REV IMMUNOL, V15, P295, DOI 10.1038/nri3824
  23. Khan WI, 2003, INFECT IMMUN, V71, P2430, DOI 10.1128/IAI.71.5.2430-2438.2003
  24. Magombedze G, 2013, FRONT PHYSIOL, V4, DOI 10.3389/fphys.2013.00206
  25. Massone C, 2010, AM J DERMATOPATH, V32, P417, DOI 10.1097/DAD.0b013e3181bb0cda
  26. Nascimento OJM, 2013, ARQ NEURO-PSIQUIAT, V71, P661, DOI 10.1590/0004-282X20130146
  27. Ogawa R, 2013, J CELL MOL MED, V17, P817, DOI 10.1111/jcmm.12060
  28. Palermo ML, 2012, AM J TROP MED HYG, V86, P878, DOI 10.4269/ajtmh.2012.12-0088
  29. Pinheiro RO, 2011, FUTURE MICROBIOL, V6, P217, DOI [10.2217/fmb.10.173, 10.2217/FMB.10.173]
  30. Ridley D S, 1966, Int J Lepr Other Mycobact Dis, V34, P255
  31. Saini C, 2013, PLOS NEGLECT TROP D, V7, DOI 10.1371/journal.pntd.0002338
  32. Schlapbach C, 2014, SCI TRANSL MED, V6, DOI 10.1126/scitranslmed.3007828
  33. Schmitt E, 2014, TRENDS IMMUNOL, V35, P61, DOI 10.1016/j.it.2013.10.004
  34. Schmitt E, 2012, J CLIN INVEST, V122, P3857, DOI 10.1172/JCI65929
  35. Quaresma JAS, 2012, MICROBES INFECT, V14, P696, DOI 10.1016/j.micinf.2012.02.010
  36. Singh TP, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0051752
  37. Stassen M, 2012, ANN NY ACAD SCI, V1247, P56, DOI 10.1111/j.1749-6632.2011.06351.x
  38. Talhari C, 2015, CLIN DERMATOL, V33, P26, DOI 10.1016/j.clindermatol.2014.07.002
  39. [Тишевская Н.В. Tishevskaya N.V.], 2015, [Российский физиологический журнал им. И.М. Сеченова, Neuroscience and Behavioral Physiology - Sechenov Physiology Journal, Rossiiskii fiziologicheskii zhurnal im. I.M. Sechenova], V101, P865
  40. Wang AX, 2015, IUBMB LIFE, V67, P601, DOI 10.1002/iub.1405
  41. Wu B, 2008, CLIN IMMUNOL, V126, P202, DOI 10.1016/j.clim.2007.09.009
  42. Zhao PC, 2013, INT IMMUNOL, V25, P547, DOI 10.1093/intimm/dxt039