Modulation of Interferon-α and Interferon-γ Receptor Expression during T-Lymphocyte Activation and Proliferation

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Abstract
Freshly isolated normal human T lymphocytes constitutively expressed receptors for interferon-α (IFN-α) and IFN-γ. Upon activation, the number of IFN-α receptors increased, paralleling the increases in cell size to give a nearly constant density of IFN-α receptors. In contrast, activation of T lymphocytes with phytohemagglutinin (PHA), concanavalin A (ConA), or phorbol myristate acetate (PMA) for 18 h decreased the specific binding of radiolabeled [Cys-Tyr-Cys] rIFN-γ to acid-washed cells. Scatchard analysis demonstrated that the decreased binding was due to a reduction in the number of high affinity IFN-γ receptors. Moreover, resting T lymphocytes had a single class of high-affinity IFN-γ receptors, whereas the activated cells appeared to have both high- and lower-affinity IFN-γ binding sites. When normalized for differences in cell size, the number of high-affinity IFN-γ receptors per unit cell surface area was approximately twofold lower on activated than on resting T lymphocytes. At least part of the decrease was due to receptor downregulation by endogenously produced IFN-γ, since monoclonal antibodies to IFN-γ prevented a large portion of the PHA-induced decrease in IFN-γ receptors.