<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Prendecki M</submitter><funding>Medical Research Council Canada</funding><funding>Kidney Research UK</funding><funding>European Research Council</funding><funding>Medical Research Council</funding><funding>UK MRC</funding><pagination>300-313</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9322550</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>257(3)</volume><pubmed_abstract>P2RX7, an ionotropic receptor for extracellular adenosine triphosphate (ATP), is expressed on immune cells, including macrophages, monocytes, and dendritic cells and is upregulated on nonimmune cells following injury. P2RX7 plays a role in many biological processes, including production of proinflammatory cytokines such as interleukin (IL)-1β via the canonical inflammasome pathway. P2RX7 has been shown to be important in inflammation and fibrosis and may also play a role in autoimmunity. We have developed and phenotyped a novel P2RX7 knockout (KO) inbred rat strain and, taking advantage of the human-resembling unique histopathological features of rat models of glomerulonephritis, we induced three models of disease: nephrotoxic nephritis, experimental autoimmune glomerulonephritis, and expe</pubmed_abstract><journal>The Journal of pathology</journal><pubmed_title>Glomerulonephritis and autoimmune vasculitis are independent of P2RX7 but may depend on alternative inflammasome pathways.</pubmed_title><pmcid>PMC9322550</pmcid><funding_grant_id>RP9/2013</funding_grant_id><funding_grant_id>ERC‐2010‐AdG_20100317</funding_grant_id><funding_grant_id>MR/M004716/1</funding_grant_id><funding_grant_id>MC_U120061454</funding_grant_id><funding_grant_id>MR/N01121X/1</funding_grant_id><funding_grant_id>MR/M018733/1</funding_grant_id><pubmed_authors>Turner-Stokes T</pubmed_authors><pubmed_authors>Unwin R</pubmed_authors><pubmed_authors>Aitman TJ</pubmed_authors><pubmed_authors>Tam FW</pubmed_authors><pubmed_authors>Woollard KJ</pubmed_authors><pubmed_authors>Pusey CD</pubmed_authors><pubmed_authors>McAdoo SP</pubmed_authors><pubmed_authors>Garcia-Diaz A</pubmed_authors><pubmed_authors>Prendecki M</pubmed_authors><pubmed_authors>Orriss I</pubmed_authors><pubmed_authors>Cook HT</pubmed_authors><pubmed_authors>Behmoaras J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Glomerulonephritis and autoimmune vasculitis are independent of P2RX7 but may depend on alternative inflammasome pathways.</name><description>P2RX7, an ionotropic receptor for extracellular adenosine triphosphate (ATP), is expressed on immune cells, including macrophages, monocytes, and dendritic cells and is upregulated on nonimmune cells following injury. P2RX7 plays a role in many biological processes, including production of proinflammatory cytokines such as interleukin (IL)-1β via the canonical inflammasome pathway. P2RX7 has been shown to be important in inflammation and fibrosis and may also play a role in autoimmunity. We have developed and phenotyped a novel P2RX7 knockout (KO) inbred rat strain and, taking advantage of the human-resembling unique histopathological features of rat models of glomerulonephritis, we induced three models of disease: nephrotoxic nephritis, experimental autoimmune glomerulonephritis, and expe</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jul</publication><modification>2026-05-27T11:48:56.232Z</modification><creation>2024-11-14T17:52:23.815Z</creation></dates><accession>S-EPMC9322550</accession><cross_references><pubmed>35239186</pubmed><doi>10.1002/path.5890</doi></cross_references></HashMap>