{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE326nnn/GSE326943/"]},"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=GSE326943"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Subclinical cholestasis is a hallmark of gut dysbiosis causing resistance to cancer immunotherapy","description":"Gut dysbiosis compromises cancer immunosurveillance by downregulating ileal mucosal addressin cell adhesion molecule 1 (MAdCAM-1) but the metabolic landscape associated with gut dysbiosis remains elusive. Here, we show that antibiotics (ABX) or ABX-associated Enterocloster species, lead to the loss of secondary cholic acid-derived bile acids, BA (DCA) and the accumulation of tauro-conjugated primary BA (TCDCA, T-abo-MCA) in the plasma of patients and mice. DCA/GDCA (glyco-DCA) compensated dysbiosis bile acid abnormalities and circumvented primary resistance to PD-1 blockade. GDCA curtailed ABX-induced MAdCAM-1 downregulation and seemed to have an impact on anti tumor immunity. The single cell RNA sequencing in a mouse model of MCA205 fibrosarcoma helped us to characterize the effect of GDCA or DCA on anti tumor immunity and showed a decrease in T cell exhaustion in the TME.","dates":{"publication":"2026/06/23"},"accession":"GSE326943","cross_references":{"GSM":["GSM9643960","GSM9643961","GSM9643959","GSM9643957","GSM9643958","GSM9643956","GSM9643962","GSM9643963"],"GPL":["28330"],"GSE":["326943"],"taxon":["Mus musculus"]}}