Regulation of mucosal IgA responses: lessons from primary immunodeficiencies.

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.

journal_name

Ann N Y Acad Sci

authors

Cerutti A,Cols M,Gentile M,Cassis L,Barra CM,He B,Puga I,Chen K

doi

10.1111/j.1749-6632.2011.06266.x

subject

Has Abstract

pub_date

2011-11-01 00:00:00

pages

132-44

eissn

0077-8923

issn

1749-6632

journal_volume

1238

pub_type

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