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Regulation of mucosal IgA responses: lessons from primary immunodeficiencies


  • Preferred citation: Cerutti, A., M. Cols, M. Gentile, L. Cassis, C.M. Barra, B. He, I. Puga & K. Chen. 2011. Regulation of mucosal IgA responses: lessons from primary immunodeficiencies. In “The Year in Human and Medical Genetics: Inborn Errors of Immunity I.” Jean-Laurent Casanova, Mary Ellen Conley & Luigi Notarangelo, Eds. Ann. N.Y. Acad. Sci.1238: 132–144.

Andrea Cerutti, Municipal Institute for Medical Research (IMIM)-Hospital del Mar, Barcelona Biomedical Research Park, Barcelona, Spain 08003. or


Adaptive co-evolution of mammals and bacteria has led to the establishment of complex commensal communities on mucosal surfaces. In spite of having available a wealth of immune-sensing and effector mechanisms capable of triggering inflammation in response to microbial intrusion, mucosal immune cells establish an intimate dialogue with microbes to generate a state of hyporesponsiveness against commensals and active readiness against pathogens. A key component of this homeostatic balance is IgA, a noninflammatory antibody isotype produced by mucosal B cells through class switching. This process involves activation of B cells by IgA-inducing signals originating from mucosal T cells, dendritic cells, and epithelial cells. Here, we review the mechanisms by which mucosal B cells undergo IgA diversification and production and discuss how the study of primary immunodeficiencies facilitates better understanding of mucosal IgA responses in humans.

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