{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Moe A"],"funding":["NIAID NIH HHS","National Heart, Lung, and Blood Institute","NHLBI NIH HHS","Minesterio de Ciencia e Innovacion/Agencia Estatal de Investigacion"],"pagination":["e175205"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11142740"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["134(11)"],"pubmed_abstract":["Neuroinflammation is a recognized complication of immunotherapeutic approaches such as immune checkpoint inhibitor treatment, chimeric antigen receptor therapy, and graft versus host disease (GVHD) occurring after allogeneic hematopoietic stem cell transplantation. While T cells and inflammatory cytokines play a role in this process, the precise interplay between the adaptive and innate arms of the immune system that propagates inflammation in the central nervous system remains incompletely understood. Using a murine model of GVHD, we demonstrate that type 2 cannabinoid receptor (CB2R) signaling plays a critical role in the pathophysiology of neuroinflammation. In these studies, we identify that CB2R expression on microglial cells induces an activated inflammatory phenotype that potentiate"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Type 2 cannabinoid receptor expression on microglial cells regulates neuroinflammation during graft-versus-host disease."],"pmcid":["PMC11142740"],"funding_grant_id":["R56 AI176611","PID2019-108992RB-I00","R01 AI148403","R01 HL154579"],"pubmed_authors":["Romero J","Hillard CJ","Moore BM","Colonna M","Cui W","Zamora AE","Szabo A","Drobyski WR","Moe A","Sauber G","Yuan CY","Rayasam A","Shah RK","Doherty A"],"additional_accession":[]},"is_claimable":false,"name":"Type 2 cannabinoid receptor expression on microglial cells regulates neuroinflammation during graft-versus-host disease.","description":"Neuroinflammation is a recognized complication of immunotherapeutic approaches such as immune checkpoint inhibitor treatment, chimeric antigen receptor therapy, and graft versus host disease (GVHD) occurring after allogeneic hematopoietic stem cell transplantation. While T cells and inflammatory cytokines play a role in this process, the precise interplay between the adaptive and innate arms of the immune system that propagates inflammation in the central nervous system remains incompletely understood. Using a murine model of GVHD, we demonstrate that type 2 cannabinoid receptor (CB2R) signaling plays a critical role in the pathophysiology of neuroinflammation. In these studies, we identify that CB2R expression on microglial cells induces an activated inflammatory phenotype that potentiate","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-04-29T14:04:20.475Z","creation":"2026-04-07T15:14:57.434Z"},"accession":"S-EPMC11142740","cross_references":{"pubmed":["38662453"],"doi":["10.1172/JCI175205"]}}