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Regulation of frontline antibody responses by innate immune signals

  • Immunology at Mount Sinai
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Abstract

Mature B cells generate protective immunity by undergoing immunoglobulin (Ig) class switching and somatic hypermutation, two Ig gene-diversifying processes that usually require cognate interactions with T cells that express CD40 ligand. This T-cell-dependent pathway provides immunological memory but is relatively slow to occur. Thus, it must be integrated with a faster, T-cell-independent pathway for B-cell activation through CD40 ligand-like molecules that are released by innate immune cells in response to microbial products. Here, we discuss recent advances in our understanding of the interplay between the innate immune system and B cells, particularly “frontline” B cells located in the marginal zone of the spleen and in the intestine.

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Acknowledgments

Supported by US National Institutes of Health grants R01 AI074378, P01 AI61093, U01 AI95613, and P01 096187 to A. Cerutti, Ministerio de Ciencia e Innovación grant SAF 2008-02725 to A. Cerutti, EUROPADnet HEALTH-F2-2008-201549 to A. Cerutti, a Sara Borrell post-doctoral fellowship to A. Chorny, and a Juan de la Cierva post-doctoral fellowships to I. Puga.

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Chorny, A., Puga, I. & Cerutti, A. Regulation of frontline antibody responses by innate immune signals. Immunol Res 54, 4–13 (2012). https://doi.org/10.1007/s12026-012-8307-5

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