{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE334nnn/GSE334457/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":[" Other","Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334457"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"L-2-Producing Tfh Cells Sustain Treg Homeostasis and Immune Tolerance in the Gut","description":"T follicular helper (Tfh) cells are well known for their role in supporting B cell responses. Here, we identify a critical B cell-independent function for Tfh cells in sustaining regulatory T (Treg) cells within gut-associated lymphoid tissues (GALT). We demonstrate that Tfh cells produce IL-2 at the T-B border and within interfollicular (IF) regions, and that this localized IL-2 is required to maintain GALT Treg homeostasis and restrain the expansion of pathogenic effector T cells. Mice selectively lacking IL-2-producing Tfh cells develop colitis and fatal multiorgan inflammation, driven by impaired GALT Treg responses and uncontrolled effector T cell activation. Broad-spectrum antibiotic treatment alleviates both intestinal and extraintestinal pathology, indicating that loss of tolerance to commensal-derived antigens is a key driver of disease. Together, these findings define a spatially restricted Tfh-derived IL-2 niche critical for GALT Treg stability and uncover an unexpected immunoregulatory role for Tfh cells in maintaining gastrointestinal tolerance beyond B cell help.","dates":{"publication":"2026/08/04"},"accession":"GSE334457","cross_references":{"GSM":["GSM9789028","GSM9789029","GSM9789026","GSM9789027","GSM9789024","GSM9789025"],"GPL":["34328"],"GSE":["334457"],"taxon":["Mus musculus"]}}