{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jakobs C"],"funding":["European Research Council"],"pagination":["e0131702"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4482750"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(6)"],"pubmed_abstract":["Mice lacking DNase II display a polyarthritis-like disease phenotype that is driven by translocation of self-DNA into the cytoplasm of phagocytic cells, where it is sensed by pattern recognition receptors. While pro-inflammatory gene expression is non-redundantly linked to the presence of STING in these mice, the contribution of the inflammasome pathway has not been explored. To this end, we studied the role of the DNA-sensing inflammasome receptor AIM2 in this self-DNA driven disease model. Arthritis-prone mice lacking AIM2 displayed strongly decreased signs of joint inflammation and associated histopathological findings. This was paralleled with a reduction of caspase-1 activation and pro-inflammatory cytokine production in diseased joints. Interestingly, systemic signs of inflammation that are associated with the lack of DNase II were not dependent on AIM2. Taken together, these data suggest a tissue-specific role for the AIM2 inflammasome as a sensor for endogenous DNA species in the course of a ligand-dependent autoinflammatory condition."],"journal":["PloS one"],"pubmed_title":["AIM2 Drives Joint Inflammation in a Self-DNA Triggered Model of Chronic Polyarthritis."],"pmcid":["PMC4482750"],"funding_grant_id":["243046"],"pubmed_authors":["Hornung V","Perner S","Jakobs C"],"additional_accession":[]},"is_claimable":false,"name":"AIM2 Drives Joint Inflammation in a Self-DNA Triggered Model of Chronic Polyarthritis.","description":"Mice lacking DNase II display a polyarthritis-like disease phenotype that is driven by translocation of self-DNA into the cytoplasm of phagocytic cells, where it is sensed by pattern recognition receptors. While pro-inflammatory gene expression is non-redundantly linked to the presence of STING in these mice, the contribution of the inflammasome pathway has not been explored. To this end, we studied the role of the DNA-sensing inflammasome receptor AIM2 in this self-DNA driven disease model. Arthritis-prone mice lacking AIM2 displayed strongly decreased signs of joint inflammation and associated histopathological findings. This was paralleled with a reduction of caspase-1 activation and pro-inflammatory cytokine production in diseased joints. Interestingly, systemic signs of inflammation that are associated with the lack of DNase II were not dependent on AIM2. Taken together, these data suggest a tissue-specific role for the AIM2 inflammasome as a sensor for endogenous DNA species in the course of a ligand-dependent autoinflammatory condition.","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015","modification":"2026-05-07T19:02:13.779Z","creation":"2019-03-26T22:54:29Z"},"accession":"S-EPMC4482750","cross_references":{"pubmed":["26114879"],"doi":["10.1371/journal.pone.0131702"]}}