Spatial Distribution of LTi-like Cells in Intestinal Mucosa Regulates Type 3 Innate Immunity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA723879 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14304912_1.fastq.gz | Fastqsanger.gz | |||
| SRR14304912_2.fastq.gz | Fastqsanger.gz | |||
| SRR14304913_1.fastq.gz | Fastqsanger.gz | |||
| SRR14304913_2.fastq.gz | Fastqsanger.gz | |||
| SRR14304914_1.fastq.gz | Fastqsanger.gz |
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Project description:Lymphoid tissue inducer (LTi)-like cells are tissue resident innate lymphocytes that rapidly secrete cytokines that promote gut epithelial integrity and protect against extracellular bacterial infections.Here, we report that the retention of LTi-like cells in conventional solitary intestinal lymphoid tissue (SILT) is essential for controlling LTi-like cell function and is maintained by expression of the chemokine receptor CXCR5. Deletion of Cxcr5 functionally unleashed LTi-like cells in a cell intrinsic manner, leading to uncontrolled IL-17 and IL-22 production. The elevated production of IL-22 in Cxcr5-deficient mice improved gut barrier integrity and protected mice during infection with the opportunistic pathogen Clostridium difficile Interestingly, Cxcr5-/- mice developed LTi-like cell aggregates that were displaced from their typical niche at the intestinal crypt, and LTi-like cell hyperresponsiveness was associated with the local formation of this unconventional SILT. Thus, LTi-like cell positioning within mucosa controls their activity via niche-specific signals that temper cytokine production during homeostasis.
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