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Ann N Y Acad Sci. 2011 Nov;1238:132-44. doi: 10.1111/j.1749-6632.2011.06266.x.

Regulation of mucosal IgA responses: lessons from primary immunodeficiencies.

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1
Municipal Institute for Medical Research-Hospital del Mar, Barcelona, Spain. acerutti@imim.es

Abstract

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.

PMID:
22129060
PMCID:
PMC3240841
DOI:
10.1111/j.1749-6632.2011.06266.x
[Indexed for MEDLINE]
Free PMC Article
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