Campylobacter infection promotes IFNγ-dependent intestinal pathology via ILC3 to ILC1 conversion.

ABSTRACT: Innate lymphoid cells (ILCs) are a heterogeneous family of immune regulators that protect against mucosal pathogens but can also promote intestinal pathology. Although the plasticity between ILCs populations has been described, the role of mucosal pathogens in inducing ILC conversion leading to intestinal pathology remains unclear. Here we demonstrate that IFNγ-producing ILCs are responsible for promoting intestinal pathology in a mouse model of enterocolitis caused by Campylobacter jejuni, a common human enteric pathogen. Phenotypic analysis revealed a distinct population of IFNγ-producing NK1.1^-T-bet⁺ILCs that accumulated in the intestine of C. jejuni-infected mice. Adoptive transfer experiments demonstrated their capacity to promote intestinal pathology. Inactivati

SUBMITTER: Muraoka WT 

PROVIDER: S-EPMC8084871 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature