Abstract

In this study we reported that on T cell receptor (TcR) gamma/delta+ cells from three cell lines Peer, MOLT-13 and ICRF-1, the T cell antigen CD7 (gp40) can be directly involved in the activation process. This is shown by a rapid increase in cytoplasmic free calcium after stimulation of these cells with an anti-CD7 monoclonal antibody (mAb). Activation through CD7 was further confirmed by measuring the production of interleukin 2 in ICRF-1 cells stimulated with anti-CD7 mAb. In addition induction of mRNA for tumor necrosis factor (TNF)-alpha and TNF-beta in Peer and for granulocyte-macrophage-colony-stimulating factor in MOLT-13 was observed in these anti-CD7-stimulated cells. The same anti-CD7 antibody was unable to activate TcR alpha/beta+ Jurkat cells or normal resting peripheral blood T lymphocytes. We further showed that normal resting TcR gamma/delta+ cells were likewise activated via the CD7 molecule. TcR gamma/delta+ cells obtained from a patient with acute lymphoblastic leukemia 3 months after autologous bone marrow transplantation were induced to proliferate, as measured by [3H]thymidine incorporation after stimulation with anti-CD7 mAb but not with anti-CD3 mAb. Interestingly TcR alpha/beta+ cells from the same donor tested in parallel were not stimulated by anti-CD7 but by anti-CD3 mAb. In essence these findings contribute to the idea that on TcR gamma/delta+ cell, the CD7 antigen could play an important role during T cell differentiation.

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