{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE341nnn/GSE341839/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE341839"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"STAT4 signaling in CD4 T cells is required for optimal Chlamydia muridarum clearance from the female reproductive tract","description":"Although the generation of Chlamydia-specific T helper Type 1 (Th1) responses is thought to be essential for Chlamydia immunity, recent studies have questioned this simple model. For example, deficiency in T-bet, or the capacity of CD4 T cells to secrete IFN-g, does not affect the rate of Chlamydia clearance from the female reproductive tract (FRT) in a mouse model of infection. Here, we examine the role of CD4 T cells in clearance using a STAT4 f/f model controlled by CD4-Cre. the absence of STAT4 from T cells significantly impaired the ability of infected mice to clear Chlamydia from the FRT. Single-cell RNA sequencing of STAT4-sufficient CD4 T cells revealed the heightened expression of cytotoxic genes when compared to STAT4-deficient CD4 T cells. Together, these data support a new model where IL-12 signaling via STAT 4STAT4 drives a cytotoxic module associated with Chlamydia immunity.","dates":{"publication":"2026/09/04"},"accession":"GSE341839","cross_references":{"GSM":["GSM9918099","GSM9918096","GSM9918097","GSM9918098"],"GPL":["34475"],"GSE":["341839"],"taxon":["Mus musculus"]}}