Journal
MUCOSAL IMMUNOLOGY
Volume 15, Issue 3, Pages 504-514Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/s41385-022-00484-0
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Funding
- Swiss National Science foundation [BSCGIO_157841/1, 310030_192490, 310030_182744, 310030_184816]
- Russian Government Program Recruitment of the Leading Scientists into the Russian Institutions of Higher Education [075-15-2021-600]
- Swiss National Science Foundation (SNF) [310030_182744, 310030_192490] Funding Source: Swiss National Science Foundation (SNF)
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This study found that eosinophils play a crucial role in the generation of newly formed specific regulatory T cells in the context of bacterial infection. Eosinophils reside in proximity to specific regulatory T cells in infected tissues and promote their expansion. Additionally, TGF-beta expressed in eosinophils is induced by bacterial contact and allergen exposure.
Eosinophils are best known for their effector functions in settings of parasitic infection or allergen challenge, but have also increasingly been implicated in immune regulation at mucosa! sites. Here, we show using bacterial infection and antigen challenge models that extrathymic Foxp3(+) regulatory T-cells that arise de novo in the context of bacterial infection require an intact eosinophil compartment. Mouse strains with a constitutive or conditional eosinophil deficiency, or with an eosinophil-specific ablation of Tgfb, lack bacterially induced neuropilin-negative, ROR gamma t-positive gastrointestinal Treg populations in models of Helicobacter pylori, Helicobacter hepaticus and Citrobacter rodentium infection, as well as in the steady state colon and upon oral ovalbumin challenge. Treg priming in lymph nodes appears not to be impaired. Eosinophil-dependent tissue-resident Tregs express CTLA4, ICOS, CD39 and T-bet in addition to ROR gamma t. Eosinophils reside in dose proximity to Tregs in infected tissues, and specifically induce the expansion of newly formed Tregs, but not conventional T-cells in vivo and in vitro. TGF-beta expression in eosinophils is induced by bacterial contact and during allergen exposure. Specific Tgfb ablation in eosinophils and the associated Treg defects result in excessive T-cell responses in the examined Th2- but not Th1-polarized settings.
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