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Abnormally expanded CD8+/Leu-7+ lymphocytes persisting in long-term bone marrow-transplanted patients are resting pre-cytotoxic T-lymphocytes.
Leroy, E; Madariaga, L; Ben Aribia, M; Mishal, Z; Theodorou, I; Rochant, H; Vernant, J P; Senik, A.
Afiliação
  • Leroy E; Laboratoire d'Immunologie Cellulaire et de Transplantation, I.R.S.C., Villejuif, France.
Exp Hematol ; 18(7): 770-4, 1990 Aug.
Article em En | MEDLINE | ID: mdl-1696205
ABSTRACT
We analyzed the functional status of the small CD8+/Leu-7+ T-lymphocytes that circulate in increased proportions in the blood of many allogeneic bone marrow transplant (BMT) patients. Purified CD8+/Leu-7+ T cells were tested for their effect on T-cell proliferative responses. In contrast to CD8+/Leu-7-T-lymphocytes, such cells behaved as suppressor cells for lectin-induced mitogenic responses of the donor's peripheral blood lymphocytes. However, they did not interfere with the in vitro responsiveness to specific stimuli such as protein purified derivative (PPD) or alloantigens. We demonstrate that CD8+/Leu-7+ T cells are resting pre-cytotoxic T-lymphocytes (CTL) that can be induced by mitogenic lectins to express their cytolytic program in a non-specific, non-major histocompatibility complex-restricted manner against phytohemagglutinin-treated lymphoblasts or K562 target cells. The lectin-triggered cytotoxicity was achieved within a few days, together with limited cell division. Our results suggest that circulating CD8+/Leu-7+ T cells from BMT recipients are in vivo primed CTL awaiting cellular activation.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Linfócitos T / Antígenos de Diferenciação de Linfócitos T / Antígenos CD / Transplante de Medula Óssea Limite: Humans Idioma: En Ano de publicação: 1990 Tipo de documento: Article
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Linfócitos T / Antígenos de Diferenciação de Linfócitos T / Antígenos CD / Transplante de Medula Óssea Limite: Humans Idioma: En Ano de publicação: 1990 Tipo de documento: Article