{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tatsuguchi T"],"funding":["P-CAEATE","Leading Advanced Projects for Medical Innovation","Japan Science and Technology Agency","Japan Society for the Promotion of Science"],"pagination":["277-289"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9020568"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["34(5)"],"pubmed_abstract":["Effective tumor immunotherapy requires physical contact of T cells with cancer cells. However, tumors often constitute a specialized microenvironment that excludes T cells from the vicinity of cancer cells, and its underlying mechanisms are still poorly understood. DOCK2 is a Rac activator critical for migration and activation of lymphocytes. We herein show that cancer-derived cholesterol sulfate (CS), a lipid product of the sulfotransferase SULT2B1b, acts as a DOCK2 inhibitor and prevents tumor infiltration by effector T cells. Using clinical samples, we found that CS was abundantly produced in certain types of human cancers such as colon cancers. Functionally, CS-producing cancer cells exhibited resistance to cancer-specific T-cell transfer and immune checkpoint blockade. Although SULT2B"],"journal":["International immunology"],"pubmed_title":["Cancer-derived cholesterol sulfate is a key mediator to prevent tumor infiltration by effector T cells."],"pmcid":["PMC9020568"],"funding_grant_id":["19H00983","JP19gm0010001","JP20cm0106362"],"pubmed_authors":["Izumi Y","Sakurai T","Hattori Y","Nakamura M","Sakamoto M","Nishimoto K","Kunimura K","Oyama M","Tatsuguchi T","Kubota N","Bamba T","Ohki T","Uruno T","Sakata D","Sugiura Y","Oki E","Fukui Y","Tahara H","Suematsu M"],"additional_accession":[]},"is_claimable":false,"name":"Cancer-derived cholesterol sulfate is a key mediator to prevent tumor infiltration by effector T cells.","description":"Effective tumor immunotherapy requires physical contact of T cells with cancer cells. However, tumors often constitute a specialized microenvironment that excludes T cells from the vicinity of cancer cells, and its underlying mechanisms are still poorly understood. DOCK2 is a Rac activator critical for migration and activation of lymphocytes. We herein show that cancer-derived cholesterol sulfate (CS), a lipid product of the sulfotransferase SULT2B1b, acts as a DOCK2 inhibitor and prevents tumor infiltration by effector T cells. Using clinical samples, we found that CS was abundantly produced in certain types of human cancers such as colon cancers. Functionally, CS-producing cancer cells exhibited resistance to cancer-specific T-cell transfer and immune checkpoint blockade. Although SULT2B","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2025-04-19T20:08:37.521Z","creation":"2025-02-19T03:27:42.038Z"},"accession":"S-EPMC9020568","cross_references":{"pubmed":["35094065"],"doi":["10.1093/intimm/dxac002"]}}