<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pistorius K</submitter><funding>Wellcome Trust</funding><pagination>103974</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9038546</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>79</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Rheumatoid arthritis (RA) is a progressive degenerative disorder that leads to joint destruction. Available treatments only target the inflammatory component with minimal impact on joint repair. We recently uncovered a previously unappreciated family of pro-resolving mediators, the maresin conjugate in tissue regeneration (MCTR), that display both immunoregulatory and tissue-protective activities. Thus, we queried whether the production of these autacoids is disrupted in RA patients and whether they can be useful in treating joint inflammation and promoting joint repair.&lt;h4>Methods&lt;/h4>Using a highly phenotyped RA cohort we evaluated plasma MCTR concentrations and correlated these to clinical markers of disease activity. To evaluate the immunoregulatory and tissue repara</pubmed_abstract><journal>EBioMedicine</journal><pubmed_title>MCTR3 reprograms arthritic monocytes to upregulate Arginase-1 and exert pro-resolving and tissue-protective functions in experimental arthritis.</pubmed_title><pmcid>PMC9038546</pmcid><funding_grant_id>107613/Z/15/Z</funding_grant_id><pubmed_authors>Souza PR</pubmed_authors><pubmed_authors>Dalli J</pubmed_authors><pubmed_authors>Pitsillides A</pubmed_authors><pubmed_authors>Gomez EA</pubmed_authors><pubmed_authors>Pistorius K</pubmed_authors><pubmed_authors>Koenis DS</pubmed_authors><pubmed_authors>Rajeeve V</pubmed_authors><pubmed_authors>Spur BW</pubmed_authors><pubmed_authors>Foster J</pubmed_authors><pubmed_authors>Rodriguez AR</pubmed_authors><pubmed_authors>Sosabowski J</pubmed_authors><pubmed_authors>Pitzalis C</pubmed_authors><pubmed_authors>Hopkinson M</pubmed_authors><pubmed_authors>Ly L</pubmed_authors></additional><is_claimable>false</is_claimable><name>MCTR3 reprograms arthritic monocytes to upregulate Arginase-1 and exert pro-resolving and tissue-protective functions in experimental arthritis.</name><description>&lt;h4>Background&lt;/h4>Rheumatoid arthritis (RA) is a progressive degenerative disorder that leads to joint destruction. Available treatments only target the inflammatory component with minimal impact on joint repair. We recently uncovered a previously unappreciated family of pro-resolving mediators, the maresin conjugate in tissue regeneration (MCTR), that display both immunoregulatory and tissue-protective activities. Thus, we queried whether the production of these autacoids is disrupted in RA patients and whether they can be useful in treating joint inflammation and promoting joint repair.&lt;h4>Methods&lt;/h4>Using a highly phenotyped RA cohort we evaluated plasma MCTR concentrations and correlated these to clinical markers of disease activity. To evaluate the immunoregulatory and tissue repara</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 May</publication><modification>2025-04-22T18:26:25.674Z</modification><creation>2025-02-19T01:23:30.119Z</creation></dates><accession>S-EPMC9038546</accession><cross_references><pubmed>35430453</pubmed><doi>10.1016/j.ebiom.2022.103974</doi></cross_references></HashMap>