Type I IFN enhances follicular B cell contribution to the T cell–independent antibody response
Copyright policy )Type I IFN enhances follicular B cell contribution to the T cell–independent antibody response
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.
- Washington University in St. Louis School of Medicine United States
- Washington State University United States
- University of Colorado System United States
- University of Colorado Denver United States
- NATIONAL JEWISH HEALTH
Antigens, Differentiation, T-Lymphocyte, 570, IgG, T-Lymphocytes, Molecular Sequence Data, Antibody Affinity, Receptors, Antigen, B-Cell, Inbred C57BL, Article, Epitopes, Mice, Antigens, CD, Lectins, Receptors, Animals, Ficoll, Lectins, C-Type, Antigens, B-Lymphocytes, C-Type, Receptors, IgG, B-Cell, Interferon-alpha, Immunoglobulin Class Switching, CD, Toll-Like Receptor 3, Mice, Inbred C57BL, Kinetics, Poly I-C, T-Lymphocyte, Differentiation, Antigen, Antibody Formation, Lymph Nodes, Spleen, Signal Transduction
Antigens, Differentiation, T-Lymphocyte, 570, IgG, T-Lymphocytes, Molecular Sequence Data, Antibody Affinity, Receptors, Antigen, B-Cell, Inbred C57BL, Article, Epitopes, Mice, Antigens, CD, Lectins, Receptors, Animals, Ficoll, Lectins, C-Type, Antigens, B-Lymphocytes, C-Type, Receptors, IgG, B-Cell, Interferon-alpha, Immunoglobulin Class Switching, CD, Toll-Like Receptor 3, Mice, Inbred C57BL, Kinetics, Poly I-C, T-Lymphocyte, Differentiation, Antigen, Antibody Formation, Lymph Nodes, Spleen, Signal Transduction
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