Regulation of mucosal IgA responses: Lessons from primary immunodeficiencies

Andrea Cerutti, Montserrat Cols, Maurizio Gentile, Linda Cassis, Carolina M. Barra, Bing He, Irene Puga, Kang Chen

Research output: Contribution to journalReview articlepeer-review

40 Scopus citations


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.

Original languageEnglish
Pages (from-to)132-144
Number of pages13
JournalAnnals of the New York Academy of Sciences
Issue number1
StatePublished - Nov 2011


  • B cells
  • Human
  • IgA
  • Immunodeficiency
  • Mucosa


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