CXCL9/Mig Mediates T cells Recruitment to Valvular Tissue Lesions of Chronic Rheumatic Heart Disease Patients

Imagem de Miniatura
Arquivos
art_PALACIOS_CXCL9_Mig_Mediates_T_cells_Recruitment_to_Valvular_2013.PDF (469.36 KB)
Citações na Scopus
32
Tipo de produção
article
Data de publicação
2013
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
SPRINGER/PLENUM PUBLISHERS
Autores
FAE, Kellen C.
OSHIRO, Sandra E.
BILATE, Angelina M. B.
THOMAZ, Petronio G.
REIS, Maxwell dos
Citação
INFLAMMATION, v.36, n.4, p.800-811, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Rheumatic fever (RF) is an autoimmune disease triggered by Streptococcus pyogenes infection frequently observed in infants from developing countries. Rheumatic heart disease (RHD), the major sequel of RF, leads to chronic inflammation of the myocardium and valvular tissue. T cells are the main population infiltrating cardiac lesions; however, the chemokines that orchestrate their recruitment are not clearly defined. Here, we investigated the expression of chemokines and chemokine receptors in cardiac tissue biopsies obtained from chronic RHD patients. Our results showed that CCL3/MIP1 alpha gene expression was upregulated in myocardium while CCL1/I-309 and CXCL9/Mig were highly expressed in valvular tissue. Auto-reactive T cells that infiltrate valvular lesions presented a memory phenotype (CD4(+)CD45RO(+)) and migrate mainly toward CXCL9/Mig gradient. Collectively, our results show that a diverse milieu of chemokines is expressed in myocardium and valvular tissue lesions and emphasize the role of CXCL9/Mig in mediating T cell recruitment to the site of inflammation in the heart.
Palavras-chave
rheumatic fever, rheumatic heart disease, chemokines, CXCL9 (Mig), valvular lesions
URI
https://observatorio.fm.usp.br/handle/OPI/1801
Referências
  1. Akashi S, 2005, TRANSPLANTATION, V80, P378, DOI 10.1097/01.tp.0000166338.99933.e1
  2. AMOILS B, 1986, CLIN EXP IMMUNOL, V66, P88
  3. BAGGIOLINI M, 1994, ADV IMMUNOL, V55, P97
  4. Bernardini G, 2000, BLOOD, V96, P4039
  5. Bonecchi R, 1998, J EXP MED, V187, P129, DOI 10.1084/jem.187.1.129
  6. Cunningham MW, 2000, CLIN MICROBIOL REV, V13, P470, DOI 10.1128/CMR.13.3.470-511.2000
  7. Cunningham MW, 2008, ADV EXP MED BIOL, V609, P29, DOI 10.1007/978-0-387-73960-1_3
  8. DAJANI AS, 1992, JAMA-J AM MED ASSOC, V268, P2069
  9. Fae KC, 2006, J IMMUNOL, V176, P5662
  10. Gross I., 1934, AM J PATHOL, V10, P467
  11. GUILHERME L, 1995, CIRCULATION, V92, P415
  12. Guilherme L, 2004, AM J PATHOL, V165, P1583, DOI 10.1016/S0002-9440(10)63415-3
  13. Guilherme L, 2000, INT IMMUNOL, V12, P1063, DOI 10.1093/intimm/12.7.1063
  14. Haque NS, 2001, BLOOD, V97, P39, DOI 10.1182/blood.V97.1.39
  15. Haque NS, 2000, CIRCULATION, V102, P786
  16. KEMENY E, 1989, CLIN IMMUNOL IMMUNOP, V52, P225, DOI 10.1016/0090-1229(89)90174-8
  17. Lee JY, 2009, INT J INFECT DIS, V13, P117, DOI 10.1016/j.ijid.2008.06.016
  18. Livak KJ, 2001, METHODS, V25, P402, DOI 10.1006/meth.2001.1262
  19. Loetscher M, 1996, J EXP MED, V184, P963, DOI 10.1084/jem.184.3.963
  20. MARBOE CC, 1985, HUM PATHOL, V16, P332, DOI 10.1016/S0046-8177(85)80227-6
  21. MILLER MD, 1989, J IMMUNOL, V143, P2907
  22. NARULA J, 1993, CIRCULATION, V88, P2198
  23. Park MK, 2002, J IMMUNOL, V169, P1433
  24. RAIZADA V, 1983, AM J MED, V74, P90, DOI 10.1016/0002-9343(83)91124-5
  25. Roberts S, 2001, J INFECT DIS, V183, P507, DOI 10.1086/318076
  26. Sallusto F, 2000, ANNU REV IMMUNOL, V18, P593, DOI 10.1146/annurev.immunol.18.1.593
  27. Schnickel GT, 2008, J IMMUNOL, V180, P4714
  28. Yoshioka M, 2006, NAT MED, V12, P1151, DOI 10.1038/nm1476
  29. Zlotnik A, 2000, IMMUNITY, V12, P121, DOI 10.1016/S1074-7613(00)80165-X

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCP
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/11
Artigos e Materiais de Revistas Científicas - LIM/19
Carregar mais