Expansion of CD8 sup + CD57 sup + T cells after allogeneic BMT is related with a low incidence of relapse and with cytomegalovirus infection

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Abstract

Summary

Peripheral blood lymphocytes of 46 recipients of lymphocyte-depleted bone marrow allografts were phenotypically analysed over a period of 1 year. We investigated the repopulation of lymphocyte subpopulations and their relation with clinical parameters such as graft-versus-host disease (GVHD), graft-versus-leukaemia and cytomegalovirus (CMV) infection. The number of repopulated T cells varied strongly between the blood samples of the recipients. In 45 percent of the recipients the number of T cells recovered to or above normal levels within 3 months after bone marrow transplantation (BMT), whereas the other recipients remained below normal up to 1 year after BMT. In recipients with a high repopulation, the CD8 sup + T-cell subset contributed more to this high repopulation than the CD4 sup + T-cell subset. We showed that the majority of T cells of these recipients expressed the alpha beta T-cell receptor, CD8, CD57 and CD11b. HLA-DR was also highly expressed reflecting the activation stage of T cells in these recipients. BMT recipients with a high repopulation of CD8 sup + T cells showed a lower incidence of leukaemic relapse than recipients with a low repopulation. The 3-year probability of relapse was 19 percent versus 64 percent (P = 0.03), respectively. The relative high number of CD8 sup + T cells at 3 months after BMT was not associated with the incidence of GVHD. In contrast, occurrence of CMV infection after BMT was significantly higher in these recipients. Our results indicate that CD8 sup + T cells, predominantly CD57 sup +, of BMT recipients with an expansion of these cells represent an in vivo activated cell population. This CD8 sup + T-cell population may consist partially of cytotoxic cells with anti-leukaemic activity as suggested by a low relapse rate. The signal for the strong expansion of these CD8 sup + CD57 sup + T cells after BMT is still unclear, but association with CMV infection suggests that viral antigens are involved.

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