B cell depletion therapy is used to treat patients with non-Hodgkin’s lymphoma and autoimmune diseases, yet how a reduction in the B cell population effects the development and maintenance of memory CD4 T cells is not fully understood. Infection models using B cell-deficient mice suggest B cells play a critical role in CD4 memory T cell development; however, it has been difficult to ascertain whether this effect is due to disrupted lymphoid architecture or a direct requirement for B cells during infection. Initial experiments demonstrate that MHCII on B cells is required for optimal CD4 T cell responses to Listeria monocytogenes (LM) infection, suggesting that B cells are essential for antigen-presentation to CD4 T cells. In order to determine the temporal requirements for B cells in the development and maintenance of memory CD4 T cells, wild-type mice were treated with anti-CD20 at different stages during LM infection. B cells are not required during the contraction and/or maintenance phases for LM-specific CD4 T cell memory responses; however, when B cells are depleted prior to CD4 T cell priming there is a reduced frequency and number of LM-specific effector and memory CD4 T cells capable of producing IFNγ and IL-2. Additionally, B cells are required for recall responses after the formation of memory CD4 T cells. These studies suggest an indispensable role for B cells in the generation of memory CD4 T cells and the initiation of robust secondary responses during infection.
- Copyright © 2013 by The American Association of Immunologists, Inc.