CD57+ T cells augment IFN‐γ production in a one‐way mixed lymphocyte reaction and their expansion after stem cell transplantation in paediatric patients
Summary To clarify the immune response of CD57+ T cells (most of them are CD8+) in peripheral blood (PB) against alloantigens in order to elucidate the T helper 1 (Th 1) immune response, we assessed the role of CD57+ T cells in IFN‐γ (one of the representative Th 1 cytokines) production in a one‐way...
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Veröffentlicht in: | Clinical and experimental immunology 2002-10, Vol.130 (1), p.162-168 |
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To clarify the immune response of CD57+ T cells (most of them are CD8+) in peripheral blood (PB) against alloantigens in order to elucidate the T helper 1 (Th 1) immune response, we assessed the role of CD57+ T cells in IFN‐γ (one of the representative Th 1 cytokines) production in a one‐way mixed lymphocyte reaction (MLR). In this study, we showed that CD57+ T cells in responder cells were essential for effective IFN‐γ production in allogeneic MLR due partly to the augmentation of the alloresponse of regular T cells. Furthermore, IFN‐γ production in MLR correlated with the proportions of CD57+ T cells in PB regardless of the responders’ age. We also showed that the extent of the expansion of CD57+ T cells in paediatric patients after haematopoietic stem cell transplantation (HSCT) was markedly lower than that in adult patients. In addition, CD57+ T cells purified and activated with a combination of cytokines showed a greater cytotoxicity than regular T cells against human umbilical vein endothelial cells. Because IFN‐γ production in one‐way MLR is a useful predictor of graft‐versus‐host disease (GVHD), especially in the acute phase that occurs after allogeneic HSCT, our findings suggested that CD57+ T cells play a role in the development of GVHD and thus may explain the reason as to why a higher donor age is associated with an increased risk of developing GVHD while, in addition, the incidence of severe GVHD in paediatric patients is lower than that in adult patients. |
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ISSN: | 0009-9104 1365-2249 |
DOI: | 10.1046/j.1365-2249.2002.01958.x |