Intragraft activation of genes encoding cytotoxic T lymphocyte effector molecules precedes the histological evidence of rejection in human cardiac transplantation

Intragraft activation of genes encoding cytotoxic T lymphocyte effector molecules precedes the histological evidence of rejection in human cardiac transplantation

Autor Shulzhenko, N. Google Scholar
Morgun, A. Google Scholar
Zheng, X. X. Google Scholar
Diniz, RVZ Google Scholar
Almeida, D. R. Google Scholar
Ma, N. Google Scholar
Strom, T. B. Google Scholar
Gerbase-DeLima, M. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Harvard Univ
Resumo Background. the purpose of the present study was to investigate transcripts of perforin, granzyme B, and Fas ligand (FasL) in heart transplants undergoing rejection.Methods. Quantitative reverse transcriptase-polymerase chain reaction was applied for mRNA detection in 29 endomyocardial biopsy specimens from 11 cardiac allograft recipients.Results. the mRNA levels of granzyme B, perforin, and FasL were higher (P<0.05) in biopsy specimens with rejection than in biopsy specimens without rejection (granzyme B, 0.53 vs. 0.09; perforin, 0.34 vs. 0; FasL, 0.57 vs. 0.36). in prerejection biopsy specimens, granzyme B and FasL levels were significantly higher than in biopsy specimens without rejection. Any two of the three transcripts were increased in 100% of prerejection, in 92% of rejection, and in 36% of no rejection biopsy specimens (P<0.04).Conclusions. the assessment of intragraft levels of cytotoxic T lymphocyte effector molecule mRNA represents a valuable tool in the monitoring of cardiac allograft rejection, especially considering the predictive value for warning of impending acute rejection.
Idioma Inglês
Data de publicação 2001-11-27
Publicado em Transplantation. Philadelphia: Lippincott Williams & Wilkins, v. 72, n. 10, p. 1705-1708, 2001.
ISSN 0041-1337 (Sherpa/Romeo, fator de impacto)
Publicador Lippincott Williams & Wilkins
Extensão 1705-1708
Fonte http://dx.doi.org/10.1097/00007890-200111270-00025
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000172614200025
Endereço permanente http://repositorio.unifesp.br/handle/11600/26666

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