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.
Regulation of mucosal IgA responses: lessons from primary immunodeficiencies
Version of Record online: 30 NOV 2011
© 2011 New York Academy of Sciences.
Annals of the New York Academy of Sciences
Volume 1238, The Year in Human and Medical Genetics: Inborn Errors of Immunity I pages 132–144, November 2011
How to Cite
Cerutti, A., Cols, M., Gentile, M., Cassis, L., Barra, C. M., He, B., Puga, I. and Chen, K. (2011), Regulation of mucosal IgA responses: lessons from primary immunodeficiencies. Annals of the New York Academy of Sciences, 1238: 132–144. doi: 10.1111/j.1749-6632.2011.06266.x
- Issue online: 30 NOV 2011
- Version of Record online: 30 NOV 2011
- B cells;
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.