Modulation of immunoglobulin isotype change by innate immune system signals

Authors

  • Irene Puga IMIM-Hospital del Mar, Parc de Recerca Biomèdica
  • Andrea Cerutti IMIM-Hospital del Mar, Parc de Recerca Biomèdica; Immunology Institute, Department of Medicine, Mount Sinai School of Medicine, EUA; Institut Català de Recerca i Estudis Avançats (ICREA)
  • Montserrat Cols Vidal Immunology Institute, Department of Medicine, Mount Sinai School of Medicine, EUA

Keywords:

B cells, immunoglobulin, class switch recombination, innate immune system, TLR, BAFF, APRIL.

Abstract

Mature B cells emerging from bone marrow further diversify their Ig genes through two antigen-dependent processes known as somatic hypermutation (SHM) and class switch recombination (CSR). These processes require AID, a DNA-editing enzyme. B cells are engaged in a T-cell-dependent (TD) antibody response against protein antigens predominantly in germinal centres. Recent evidence shows that B cells receive additional help from invariant natural killer T cells, dendritic cells and various granulocytes, including neutrophils, eosinophils and basophils. These innate immune cells enhance T-cell-dependent antibody responses by delivering B-cell helper signals both in the germinal centre and at postgerminal centre lymphoid sites such as the bone marrow. In addition to enhancing and complementing the B-cell helper activity of canonical T cells, invariant natural killer T cells, dendritic cells and granulocytes can deliver T-cell-independent B-cell helper signals at the mucosal interface and in the marginal zone of the spleen to initiate rapid innate-like antibody responses. In this paper we discuss recent advances in the role of innate cells in B-cell helper signals and in antibody diversification and production.

Key words: B cells, immunoglobulin, class switch recombination, innate
immune system, TLR, BAFF, APRIL.

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