Transferrin Receptor Induction in Mitogen-Stimulated Human T Lymphocytes Is Required for DNA Synthesis and Cell Division and Is Regulated by Interleukin-2 (TCGF)
Since the discovery of T-cell growth factor (TCGF, IL-2) by Gallo and co-workers nearly 8 years ago (Morgan et al., 1976), much interest has been focused on its ability to support the long-term growth of activated T lymphocytes (Ruscetti et al., 1977; Mier and Gallo, 1980). At the same time, others have shown that lymphocyte proliferation is dependent on transferrin, a major serum glycoprotein (Dillner-Centerlind et al., 1979). Because both transferrin and TCGF exert their effects through interaction with cell surface receptors (Robb et al., 1981; Neckers and Cossman, 1983), it is of interest that resting lymphocytes do not express receptors for either substance (Smith et al., 1979; Tormey et al., 1972; Larrick and Cresswell, 1979). Making use of recently available monoclonal antibodies which recognize each receptor (Goding and Burns, 1981; Sutherland et al., 1981; Uchiyama et al., 1981a,b; Trowbridge and Lopez, 1982; Leonard et al., 1982), we have investigated the sequence of events in which lymphocytes become responsive to both TCGF and transferrin. In the course of these experiments we have determined that the mitogenic potential of TCGF is dependent on transferrin receptor appearance on T cells and that TCGF receptor stability is also dependent on maintenance of transferrin receptor expression.
KeywordsTransferrin Receptor Stimulation Index Peripheral Blood Mononuclear Normal Human Bone Marrow Transferrin Receptor Expression
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