Defective IgA response to atypical intestinal commensals in IL-21 receptor deficiency reshapes immune cell homeostasis and mucosal immunity View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-01

AUTHORS

Hyeseon Cho, Henrique Jaime, Rafael Pires de Oliveira, Byunghyun Kang, Rosanne Spolski, Tina Vaziri, Timothy G. Myers, Vishal Thovarai, Zeli Shen, James G. Fox, Warren J. Leonard, Brian L. Kelsall

ABSTRACT

Despite studies indicating the effects of IL-21 signaling in intestinal inflammation, its roles in intestinal homeostasis and infection are not yet clear. Here, we report potent effects of commensal microbiota on the phenotypic manifestations of IL-21 receptor deficiency. IL-21 is produced highly in the small intestine and appears to be critical for mounting an IgA response against atypical commensals such as segmented filamentous bacteria and Helicobacter, but not to the majority of commensals. In the presence of these atypical commensals, IL-21R-deficient mice exhibit reduced numbers of germinal center and IgA+ B cells and expression of activation-induced cytidine deaminase in Peyer's patches as well as a significant decrease in small intestine IgA+ plasmablasts and plasma cells, leading to higher bacterial burdens and subsequent expansion of Th17 and Treg cells. These microbiota-mediated secondary changes in turn enhance T cell responses to an oral antigen and strikingly dampen Citrobacter rodentium-induced immunopathology, demonstrating a complex interplay between IL-21-mediated mucosal immunity, microbiota, and pathogens. More... »

PAGES

85-96

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41385-018-0056-x

DOI

http://dx.doi.org/10.1038/s41385-018-0056-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1106023260

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30087442


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