{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["McCoy SS"],"funding":["National Center for Advancing Translational Sciences","NCATS NIH HHS","NIDCR NIH HHS","NIDDK NIH HHS","Clinical and Translational Science Award","NIH","NIDDK"],"pagination":["4207-4218"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9536796"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["61(10)"],"pubmed_abstract":["<h4>Objectives</h4>Sjögren's disease (SjD) is a systemic autoimmune disease characterized by focal lymphocytic infiltrate of salivary glands (SGs) and high SG IFNγ, both of which are associated with elevated lymphoma risk. IFNγ is also biologically relevant to mesenchymal stromal cells (MSCs), a SG resident cell with unique niche regenerative and immunoregulatory capacities. In contrast to the role of IFNγ in SjD, IFNγ promotes an anti-inflammatory MSC phenotype in other diseases. The objective of this study was to define the immunobiology of IFNγ-exposed SG-MSCs with and without the JAK1 & 2 inhibitor, ruxolitinib.<h4>Methods</h4>SG-MSCs were isolated from SjD and controls human subjects. SG-MSCs were treated with 10 ng/ml IFNγ +/- 1000 nM ruxolitinib. Experimental methods included flow c"],"journal":["Rheumatology (Oxford, England)"],"pubmed_title":["Ruxolitinib inhibits IFNγ-stimulated Sjogren's salivary gland MSC HLA-DR expression and chemokine-dependent T cell migration."],"pmcid":["PMC9536796"],"funding_grant_id":["R01DK109508","R01 DK109508","KL2 TR002374","R03 DE031340","1KL2TR002374"],"pubmed_authors":["McCoy SS","Parker M","Das R","Pennati A","Gurevic I","Galipeau J"],"additional_accession":[]},"is_claimable":false,"name":"Ruxolitinib inhibits IFNγ-stimulated Sjogren's salivary gland MSC HLA-DR expression and chemokine-dependent T cell migration.","description":"<h4>Objectives</h4>Sjögren's disease (SjD) is a systemic autoimmune disease characterized by focal lymphocytic infiltrate of salivary glands (SGs) and high SG IFNγ, both of which are associated with elevated lymphoma risk. IFNγ is also biologically relevant to mesenchymal stromal cells (MSCs), a SG resident cell with unique niche regenerative and immunoregulatory capacities. In contrast to the role of IFNγ in SjD, IFNγ promotes an anti-inflammatory MSC phenotype in other diseases. The objective of this study was to define the immunobiology of IFNγ-exposed SG-MSCs with and without the JAK1 & 2 inhibitor, ruxolitinib.<h4>Methods</h4>SG-MSCs were isolated from SjD and controls human subjects. SG-MSCs were treated with 10 ng/ml IFNγ +/- 1000 nM ruxolitinib. Experimental methods included flow c","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2025-04-19T13:32:54.385Z","creation":"2024-11-21T06:32:42.048Z"},"accession":"S-EPMC9536796","cross_references":{"pubmed":["35218354"],"doi":["10.1093/rheumatology/keac111"]}}