<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE341nnn/GSE341839/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE341839</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>STAT4 signaling in CD4 T cells is required for optimal Chlamydia muridarum clearance from the female reproductive tract</name><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.</description><dates><publication>2026/09/04</publication></dates><accession>GSE341839</accession><cross_references><GSM>GSM9918099</GSM><GSM>GSM9918096</GSM><GSM>GSM9918097</GSM><GSM>GSM9918098</GSM><GPL>34475</GPL><GSE>341839</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>