{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He JY"],"funding":["Parker Institute for Cancer Immunotherapy","Kenneth Rainin Foundation","Crohn’s and Colitis Foundation","NIDDK NIH HHS","Burroughs Wellcome Fund","NIAID NIH HHS","NCI NIH HHS","National Institutes of Health","UCSF ImmunoX","V Foundation for Cancer Research","Damon Runyon Cancer Research Foundation"],"pagination":["e008628"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11033653"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(4)"],"pubmed_abstract":["<h4>Background</h4>Colitis caused by checkpoint inhibitors (CPI) is frequent and is treated with empiric steroids, but CPI colitis mechanisms in steroid-experienced or refractory disease are unclear.<h4>Methods</h4>Using colon biopsies and blood from predominantly steroid-experienced CPI colitis patients, we performed multiplexed single-cell transcriptomics and proteomics to nominate contributing populations.<h4>Results</h4>CPI colitis biopsies showed enrichment of CD4<sup>+</sup>resident memory (RM) T cells in addition to CD8<sup>+</sup> RM and cytotoxic CD8<sup>+</sup> T cells. Matching T cell receptor (TCR) clonotypes suggested that both RMs are progenitors that yield cytotoxic effectors. Activated, CD38<sup>+</sup> HLA-DR<sup>+</sup> CD4<sup>+</sup> RM and cytotoxic CD8<sup>+</sup> T c"],"journal":["Journal for immunotherapy of cancer"],"pubmed_title":["Dysregulation of CD4&lt;sup&gt;+&lt;/sup&gt; and CD8&lt;sup&gt;+&lt;/sup&gt; resident memory T, myeloid, and stromal cells in steroid-experienced, checkpoint inhibitor colitis."],"pmcid":["PMC11033653"],"funding_grant_id":["N/A","K08AI139375","K08 DK123202","T2023-011","R35 CA253175","Career Award for Medical Scientists","CoPilot Award","CI 110-21","K08 AI139375","K08DK123202","KRA000152","Career Development Award"],"pubmed_authors":["Yang H","Bain J","Pisco AO","Zhang L","Combes AJ","Fong L","Shi Y","Law K","Fan F","Mennillo E","Shen A","Oh DY","Davidson B","He JY","Kim YJ","Rao AA","Kattah MG","Kushnoor D","Rusu I","Cheung A","Andersen C","Tsui J"],"additional_accession":[]},"is_claimable":false,"name":"Dysregulation of CD4&lt;sup&gt;+&lt;/sup&gt; and CD8&lt;sup&gt;+&lt;/sup&gt; resident memory T, myeloid, and stromal cells in steroid-experienced, checkpoint inhibitor colitis.","description":"<h4>Background</h4>Colitis caused by checkpoint inhibitors (CPI) is frequent and is treated with empiric steroids, but CPI colitis mechanisms in steroid-experienced or refractory disease are unclear.<h4>Methods</h4>Using colon biopsies and blood from predominantly steroid-experienced CPI colitis patients, we performed multiplexed single-cell transcriptomics and proteomics to nominate contributing populations.<h4>Results</h4>CPI colitis biopsies showed enrichment of CD4<sup>+</sup>resident memory (RM) T cells in addition to CD8<sup>+</sup> RM and cytotoxic CD8<sup>+</sup> T cells. Matching T cell receptor (TCR) clonotypes suggested that both RMs are progenitors that yield cytotoxic effectors. Activated, CD38<sup>+</sup> HLA-DR<sup>+</sup> CD4<sup>+</sup> RM and cytotoxic CD8<sup>+</sup> T c","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-06-08T06:04:15.744Z","creation":"2026-06-08T03:14:26.326Z"},"accession":"S-EPMC11033653","cross_references":{"pubmed":["38642938"],"doi":["10.1136/jitc-2023-008628"]}}