Regulatory T cells suppress virus-specific antibody responses to Friend retrovirus infection.

Abstract

Recent vaccine studies with experimental antigens have shown that regulatory T cells (Tregs) constrain the magnitude of B cell responses. This homeostatic Treg-mediated suppression is thought to reduce the potential of germinal center (GC) responses to generate autoreactive antibodies. However, essentially opposite results were observed in live influenza infections where Tregs promoted B cell and antibody responses. Thus, it remains unclear whether Tregs dampen or enhance B cell responses, especially during live viral infections. Here, we use mice infected with Friend retrovirus (FV), which induces a robust expansion of Tregs. Depletion of Tregs led to elevated activation, proliferation, and class switching of B cells. In addition, Treg depletion enhanced the production of virus-specific and virus-neutralizing antibodies and reduced FV viremia. Thus, in contrast to influenza infection, Tregs either directly or indirectly suppress B cells during mouse retroviral infection indicating that the ultimate effect of Tregs on B cell responses is specific to the particular infectious agent.