Measles virus infection of human T cells modulates cytokine generation and IL-2 receptor alpha chain expression.

Measles virus (MV) suppresses specific functions in cells of the immune system and causes a generalized immunosuppression by mechanisms which remain undefined. It has been previously established that mitogen-induced proliferation of peripheral blood mononuclear cells (PBMC) is suppressed by infection with MV. Our current study demonstrates that MV infection inhibits antigen-specific proliferation of T lymphocytes. The inhibition of proliferation was not due to a decrease in IL-2 production. IL-2 production in cultures of infected and uninfected antigen-specific T cells was similar. In contrast, we found that expression of the IL-2R alpha subunit was decreased in mitogen-stimulated, MV-infected PBMC and antigen-stimulated, MV-infected T lymphocytes compared to stimulated but noninfected T cells. However, the expression of the IL-2R beta subunit was not altered in MV-infected T cells. We also examined the influence of MV infection on the production of the cytokines IL-4, IL-6, IL-10, and IFN-gamma by T lymphocytes. By comparing infected versus uninfected antigen-specific T cell lines, we found that MV infection of antigen-specific activated T cells caused no substantial change in generation of IFN-gamma, IL-6, or IL-10. There was a 50% reduction in IL-4 generation following MV infection. These data indicate that the immunosuppression by acute MV infection is not associated with a generalized inhibition of cytokine production. One mechanism for the suppression of proliferation following acute MV infection may be a block in the expression of the IL-2R alpha subunit by activated T cells.