Jared Klarquist 1, Eric W Cross 2, Scott B Thompson 2, Benjamin Willett 2, Daniel L Aldridge 3, Alayna K Caffrey-Carr 2, Zhenming Xu 4, Christopher A Hunter 3, Andrew Getahun 2, Ross M Kedl 5
Klairquist et al. showed that, compared to wild-type (WT) mice, mice lacking B cells (μMT) or with B cells specific to an irrelevant antigen (MD4) showed a deficient antigen-specific CD8+ T cell response after subunit vaccination, but not infection. This difference was not due to B cell antibody production or antigen presentation, or indirectly through CD4+ T cells, but rather through B cell IL-27 production. Antigen-specific CD8+ T cells from MD4 mice, relative to WT mice, showed poorer cytokine production, increased effector phenotype, reduced persistence of memory T cells, and impaired protection from infection.
Contributed by Alex Najibi
Jared Klarquist 1, Eric W Cross 2, Scott B Thompson 2, Benjamin Willett 2, Daniel L Aldridge 3, Alayna K Caffrey-Carr 2, Zhenming Xu 4, Christopher A Hunter 3, Andrew Getahun 2, Ross M Kedl 5
Klairquist et al. showed that, compared to wild-type (WT) mice, mice lacking B cells (μMT) or with B cells specific to an irrelevant antigen (MD4) showed a deficient antigen-specific CD8+ T cell response after subunit vaccination, but not infection. This difference was not due to B cell antibody production or antigen presentation, or indirectly through CD4+ T cells, but rather through B cell IL-27 production. Antigen-specific CD8+ T cells from MD4 mice, relative to WT mice, showed poorer cytokine production, increased effector phenotype, reduced persistence of memory T cells, and impaired protection from infection.
Contributed by Alex Najibi
ABSTRACT: 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.
Author Info: (1) Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA. Electronic address: jared.klarquist@cuanschutz.edu. (2) Department
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Author Info: (1) Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA. Electronic address: jared.klarquist@cuanschutz.edu. (2) Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA. (3) University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, USA. (4) 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. (5) Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA. Electronic address: ross.kedl@cuanschutz.edu.
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Citation: Cell Rep. 2021 Aug 24