Virus-induced interferon α β (IFN- α β) production by T cells and by Th1 and Th2 helper T cell clones: A study of the immunoregulatory actions of IFN-γ versus IFN- α β on functions of different T cell populations

Spleen cells, resting T cells, activated T cells, and T cell clones characterized as type 1 (Th1) and type 2 (Th2) were investigated for their ability to produce interferon (IFN) following in vitro culture with Newcastle disease virus (NDV). All of the above cell populations, including both Th1 and Th2 T cell clones, produced high levels of IFN following in vitro culture with NDV. This IFN was characterized as a mixture of IFN-α and IFN-β with IFN-α being the predominate species of IFN contained in the mixture. IL-2 greatly enhanced the production of IFN- α β by all cell populations in response to NDV. These different T cell populations responded very differently to the immunoregulatory actions of IFN-γ versus IFN- α β. IFN- α β was shown to be a potent inhibitor of Con A or IL-2-induced proliferation of different T cell populations. This inhibition was not associated with a reduction in lymphokine production since spleen cells or Th1 T cell clones cultured with Con A and IFN- α β had no decrease in IL-2 or IFN-γ production when compared to Con A-stimulated control cultures. IFN-γ had little to no inhibitory activity on Con A-induced proliferation of spleen cells. In fact, Con A-induced proliferation was usually enhanced by IFN-γ when nylon wool-enriched T cells were assessed. Different results were observed when IFN-γ and IFN- α β were investigated for their ability to inhibit IL-2-induced proliferation of different T helper cell clones. IFN-γ and IFN- α β were both capable of inhibiting IL-2-induced proliferation of T cell clones characterized as type 2 (Th2). In contrast, IFN-γ had no effect on IL-2-induced proliferation of Th1 clones. IFN- α β, however, inhibited IL-2-induced proliferative responses of both Th1 and Th2 T cell clones. These results document the facts that (1) IFN-γ and IFN- α β differ in their immunoregulatory actions, (2) different T cell subpopulations vary in their susceptibility to IFN-γ regulation, and (3) virus induction of IFN- α β appears to be a ubiquitous function associated with different T cell populations.