The Group 3 Innate Lymphoid Cell Defect in Aryl Hydrocarbon Receptor Deficient Mice Is Associated with T Cell Hyperactivation during Intestinal Infection. Academic Article uri icon

Overview

abstract

  • Intestinal infection with the intracellular parasite Toxoplasma gondii results in the translocation of commensal bacteria to peripheral organs and the development of a T cell response specific to the microbiota. In naïve mice, the recently described RORγt+ group 3 innate lymphoid cell (ILC) population plays a critical role in promoting intestinal barrier function and limiting responses to gut-resident commensal bacteria. Given this role for group 3 ILCs, studies were performed to evaluate whether these cells might influence the immune response to mucosal infection with T. gondii. Phenotypic characterization of RORγt+ ILCs in T. gondii infected mice revealed that this population decreased following challenge but the population that remained expressed costimulatory molecules and IL-22. One factor that influences the maintenance of RORγt+ ILCs is the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, and Ahr-/- mice have a marked defect in the lamina propria group 3 ILC population. When Ahr-/- mice were challenged with T. gondii, they lost more weight than wild type controls. This disease course in Ahr-/- animals was associated with increased T cell responses to Toxoplasma antigen and crude commensal antigen preparations. Together, these data suggest that group 3 ILCs have a role in limiting T cell activation during intestinal infection.

publication date

  • May 26, 2015

Research

keywords

  • Basic Helix-Loop-Helix Transcription Factors
  • Intestinal Diseases
  • Receptors, Aryl Hydrocarbon
  • T-Lymphocytes
  • Toxoplasmosis, Animal

Identity

PubMed Central ID

  • PMC4444139

Scopus Document Identifier

  • 84956601825

Digital Object Identifier (DOI)

  • 10.1038/nature13684

PubMed ID

  • 26010337

Additional Document Info

volume

  • 10

issue

  • 5