B cells promote CD8 T cell primary and memory responses to subunit vaccines
Jared Klarquist,
Eric W. Cross,
Scott B. Thompson,
Benjamin Willett,
Daniel L. Aldridge,
Alayna K. Caffrey-Carr,
Zhenming Xu,
Christopher A. Hunter,
Andrew Getahun,
Ross M. Kedl
Affiliations
Jared Klarquist
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA; Corresponding author
Eric W. Cross
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA
Scott B. Thompson
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA
Benjamin Willett
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA
Daniel L. Aldridge
University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, USA
Alayna K. Caffrey-Carr
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA
Zhenming Xu
Department of Microbiology, Immunology and Molecular Genetics, The Joe R. & Teresa Lozano Long School of Medicine, University of Texas Health Science Center San Antonio, San Antonio, TX 78229, USA
Christopher A. Hunter
University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, USA
Andrew Getahun
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA
Ross M. Kedl
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA; Corresponding author
Summary: The relationship between B cells and CD4 T cells has been carefully studied, revealing a collaborative effort in which B cells promote the activation, differentiation, and expansion of CD4 T cells while the so-called “helper” cells provide signals to B cells, influencing their class switching and fate. Interactions between B cells and CD8 T cells are not as well studied, although CD8 T cells exhibit an accelerated contraction after certain infections in B-cell-deficient mice. Here, we find that B cells significantly enhance primary CD8 T cell responses after vaccination. Moreover, memory CD8 numbers and function are impaired in B-cell-deficient animals, leading to increased susceptibility to bacterial challenge. We also show that interleukin-27 production by B cells contributes to their impact on primary, but not memory, CD8 responses. Better understanding of the interactions between CD8 T cells and B cells may aid in the design of more effective future vaccine strategies.
