Type I IFN enhances follicular B cell contribution to the T cell–independent antibody response

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  • Cristina L. Swanson
    Integrated Department of Immunology, University of Colorado, Denver, and National Jewish Health, Denver, CO 80206 1
  • Timothy J. Wilson
    Department of Pathology and Immunology, Washington University, St. Louis, MO 63110 2
  • Pamela Strauch
    Integrated Department of Immunology, University of Colorado, Denver, and National Jewish Health, Denver, CO 80206 1
  • Marco Colonna
    Department of Pathology and Immunology, Washington University, St. Louis, MO 63110 2
  • Roberta Pelanda
    Integrated Department of Immunology, University of Colorado, Denver, and National Jewish Health, Denver, CO 80206 1
  • Raul M. Torres
    Integrated Department of Immunology, University of Colorado, Denver, and National Jewish Health, Denver, CO 80206 1

Abstract

<jats:p>Humoral immunity to viruses and encapsulated bacteria is comprised of T cell–independent type 2 (TI-2) antibody responses that are characterized by rapid antibody production by marginal zone and B1 B cells. We demonstrate that toll-like receptor (TLR) ligands influence the TI-2 antibody response not only by enhancing the overall magnitude but also by skewing this response to one that is dominated by IgG isotypes. Importantly, TLR ligands facilitate this response by inducing type I interferon (IFN), which in turn elicits rapid and significant amounts of antigen-specific IgG2c predominantly from FO (follicular) B cells. Furthermore, we show that although the IgG2c antibody response requires B cell–autonomous IFN-α receptor signaling, it is independent of B cell–intrinsic TLR signaling. Thus, innate signals have the capacity to enhance TI-2 antibody responses by promoting participation of FO B cells, which then elaborate effective IgG anti-pathogen antibodies.</jats:p>

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