B cell derived type I interferon promotes T cell effector function during chronic infection

However, their impact on T cell responses, in particular of CD8+ T cells, remains incompletely understood. Here, we identify a critical role for B cells in promoting CD8+ T cell responses to chronic, but not to acute, viral infections.

We identify B cells as key type I interferon (IFN-I) producers and demonstrate that the T cell requirement for B cell-derived IFN-I is cell-intrinsically regulated by T cell receptor (TCR) stimulation, with T cells encountering high antigen loads showing an increased dependency on IFN-I to acquire effector function. In the absence of B cells, exhausted T cells displayed more severe functional impairments in effector differentiation and cytokine production, resembling tolerized T cells.