Interferon‐γ is not an antiviral, but a growth‐promoting factor for t lymphocytes

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Abstract
The effects of interferon (1FN)-γ or IFN-α/β on virus yield, (2′-5′)oligo(A) synthetase activation, H-2 antigen expression and proliferation of T lymphocytes have been investigated. Under the culture conditions used, vesicular stomatitis virus or Semliki Forest virus replication in T cells was not impaired by the addition of IFN-γ, whereas it was completely inhibited by the addition of IFN-α/β. In contrast, B cell lines, macrophage-transformed cell lines and fibroblasts were fully protected by both IFN-γ as well as IFN-α/β following virus infection. The lack of sensitivity of T lymphocytes to the antiviral effects of IFN-γ was not due to absence of specific membrane receptors, since in saturation binding experiments with 125I-labeled murine IFN-γ most T cell lines displayed a number of binding sites and a degree of affinity comparable to those found on B cells, which are fully sensitive to IFN-γ antiviral activity. Analysis of IFN-induced dsRNA-dependent (2′-5′)oligo(A) synthetase activity, one of the biochemical markers for cellular responses to IFN, showed that it was not induced in T lymphocytes after IFN-γ treatment, whereas IFN-α/β induced high levels. Both IFN-γ and IFN-α/β enhanced H-2 antigen expression on T cells as well as on cells of different histological type. Moreover, when IFN-γ was tested for its antiproliferative activity on T cells, it was found to consistently potentiate the response of these cells to mitogens or growth factors, rather than inhibit their proliferation. Taken as a whole these results suggest that on T lymphocytes IFN-γ should not be regarded as an antiviral agent, but rather as a modulator of T cell growth and functional differentiation, transducing intracellular signals dissimilar to those observed with target cells of different origin.