Abstract
In addition to monoclonal antibodies against the CD3 (T3)-T-cell antigen receptor (CD3/Ti) complex1–3, several other monoclonals directed towards distinct cell surface structures on human (CD2 (T11)4 and Tp445,6) and murine (Thy-17–9, TAP10, and Ly-611) T lymphocytes are capable of activating T cells. It has been proposed that such structures may function as alternative pathways of stimulation. To examine directly whether any relationship exists between Thy-1-dependent activation phenomena and T-cell activation mediated through the CD3/Ti complex, we have transfected several CD3/Ti– variants12,13 of the human T-cell line Jurkat with the murine Thy-1.2 gene. Our data indicate that in CD3/Ti–, Thy-1.2+ transfectants, monoclonal antibodies against Thy-1.2 can induce a rise in cytoplasmic free calcium ([Ca2+]i), but fail to stimulate interleukin-2 (IL-2) production. The only defect in these variant cell lines responsible for the inability to produce IL-2 in response to Thy-1 stimulation was in the expression of the CD3/Ti complex, because replacement of defective Ti α- or β-chain genes reconstributed both surface expression of CD3/Ti and responsiveness to Thy-1 in the IL-2 production assay.
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Gunter, K., Germain, R., Kroczek, R. et al. Thy-1-mediated T-cell activation requires co-expression of CD3/Ti complex. Nature 326, 505–507 (1987). https://doi.org/10.1038/326505a0
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DOI: https://doi.org/10.1038/326505a0
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