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 immun e system and causes a generalized immunosuppression by mechanisms whic h remain undefined. II has been previously established that mitogen-in duced proliferation of peripheral blood mononuclear cells (PBMC) is su ppressed by infection with MV. Our current study demonstrates that MV infection inhibits antigen-specific proliferation of T lymphocytes. Th e inhibition of proliferation was not due to a decrease in IL-2 produc tion. IL-2 production in cultures of infected and uninfected antigen-s pecific T cells was similar. In contrast, we found that expression of the lL-2R alpha subunit was decreased in mitogen-stimulated, MV-infect ed 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 examin ed 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 inf ection of antigen-specific activated T cells caused no substantial cha nge in generation of IFN-gamma, IL-6, or IL-10. There was a 50% reduct ion in IL-4 generation following MV infection. These data indicate tha t 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 blo ck in the expression of the IL-2R alpha subunit by activated T cells. (C) 1997 Academic Press.