CD4 T cell-mediated control of a γ-herpesvirus in B cell-deficient mice is mediated by IFN-γ

Abstract

The lack of B cells and antibody does not prevent mice from dealing effectively with a pathogenic γ-herpesvirus. Both CD4+ and CD8+ T cells contribute to the control of virus replication in the respiratory tract, with the depletion of either lymphocyte subset leading to increased titers in the lung. However, the further neutralization of IFN-γ diminishes the effectiveness of the CD4+ T cell response and causes substantially increased mortality. Experiments with bone marrow radiation chimeras indicate that the immune CD4+ effectors operate optimally when there is the potential for direct interaction with virus-infected targets expressing MHC class II glycoproteins, suggesting that the IFN-γ p..