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
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- Timothy J. Wilson
- Department of Pathology and Immunology, Washington University, St. Louis, MO 63110 2
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- Pamela Strauch
- Integrated Department of Immunology, University of Colorado, Denver, and National Jewish Health, Denver, CO 80206 1
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- Marco Colonna
- Department of Pathology and Immunology, Washington University, St. Louis, MO 63110 2
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- Roberta Pelanda
- Integrated Department of Immunology, University of Colorado, Denver, and National Jewish Health, Denver, CO 80206 1
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- Raul M. Torres
- Integrated Department of Immunology, University of Colorado, Denver, and National Jewish Health, Denver, CO 80206 1
抄録
<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>
収録刊行物
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- Journal of Experimental Medicine
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Journal of Experimental Medicine 207 (7), 1485-1500, 2010-06-21
Rockefeller University Press