<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Moe A</submitter><funding>NIAID NIH HHS</funding><funding>National Heart, Lung, and Blood Institute</funding><funding>NHLBI NIH HHS</funding><funding>Minesterio de Ciencia e Innovacion/Agencia Estatal de Investigacion</funding><pagination>e175205</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11142740</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>134(11)</volume><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</pubmed_abstract><journal>The Journal of clinical investigation</journal><pubmed_title>Type 2 cannabinoid receptor expression on microglial cells regulates neuroinflammation during graft-versus-host disease.</pubmed_title><pmcid>PMC11142740</pmcid><funding_grant_id>R56 AI176611</funding_grant_id><funding_grant_id>PID2019-108992RB-I00</funding_grant_id><funding_grant_id>R01 AI148403</funding_grant_id><funding_grant_id>R01 HL154579</funding_grant_id><pubmed_authors>Romero J</pubmed_authors><pubmed_authors>Hillard CJ</pubmed_authors><pubmed_authors>Moore BM</pubmed_authors><pubmed_authors>Colonna M</pubmed_authors><pubmed_authors>Cui W</pubmed_authors><pubmed_authors>Zamora AE</pubmed_authors><pubmed_authors>Szabo A</pubmed_authors><pubmed_authors>Drobyski WR</pubmed_authors><pubmed_authors>Moe A</pubmed_authors><pubmed_authors>Sauber G</pubmed_authors><pubmed_authors>Yuan CY</pubmed_authors><pubmed_authors>Rayasam A</pubmed_authors><pubmed_authors>Shah RK</pubmed_authors><pubmed_authors>Doherty A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Type 2 cannabinoid receptor expression on microglial cells regulates neuroinflammation during graft-versus-host disease.</name><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</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-04-29T14:04:20.475Z</modification><creation>2026-04-07T15:14:57.434Z</creation></dates><accession>S-EPMC11142740</accession><cross_references><pubmed>38662453</pubmed><doi>10.1172/JCI175205</doi></cross_references></HashMap>