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National Academy of Sciences, Proceedings of the National Academy of Sciences, 35(112), p. 11024-11029, 2015

DOI: 10.1073/pnas.1503315112

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IL-22 regulates lymphoid chemokine production and assembly of tertiary lymphoid organs

Journal article published in 2015 by Maria de la Luz Garcia-Hernandez, Francesca Barone, S. Nayara, Saba Nayar, Joana Campos, J. Camposa, Thomas Cloake, T. Cloakea, David R. Withers ORCID, Kai-Michael Toellner, Yang Zhang, Lynette Fouser, Benjamin Fisher, Javier Rangel-Moreno ORCID, Simon Bowman and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

The series of events leading to tertiary lymphoid organ (TLO) formation in mucosal organs following tissue damage remain unclear. Using a virus-induced model of autoantibody formation in the salivary glands of adult mice, we demonstrate that IL-22 provides a mechanistic link between mucosal infection, B-cell recruitment, and humoral autoimmunity. IL-22 receptor engagement is necessary and sufficient to promote differential expression of chemokine (C-X-C motif) ligand 12 and chemokine (C-X-C motif) ligand 13 in epithelial and fibroblastic stromal cells that, in turn, is pivotal for B-cell recruitment and organization of the TLOs. Accordingly, genetic and therapeutic blockade of IL-22 impairs and reverses TLO formation and autoantibody production. Our work highlights a critical role for IL-22 in TLO-induced pathology and provides a rationale for the use of IL-22-blocking agents in B-cell-mediated autoimmune conditions.