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- W4313356570 abstract "Abstract Inhibitor of DNA binding 1 (Id1) is a nuclear transcription factor that is primarily fibroblast derived with elevated expression in rheumatoid arthritis (RA) synovial tissues (STs) and synovial fluids (SFs). Id1 is potently angiogenic in RA, and targeting Id1 or its signaling pathways may attenuate unwanted inflammatory outcomes. Cell signaling studies showed that Id1 can upregulate Jnk in FLS, human dermal microvascular endothelial cells, and endothelial progenitor cells and that Jnk could be targeted to reduce angiogenic responses in vivo. We also showed Id1 can be citrullinated and serve as an autoantigen by inducing anti-citrullinated protein antibodies (ACPAs) in RA peripheral blood (PB) sera and SFs. ELISA for Id1 was performed on exosomes isolated from RA, osteoarthritis, and normal (NL) FLS supernatants. RA FLS were transfected with a clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 plasmid targeting the Id1 gene. Lastly, immunodot blots (IDB) were performed on NL and RA PB sera and SFs to test the presence of ACPAs to citrullinated Id1 (citId1). Exosome analysis showed >80% of Id1 detected in RA FLS supernatants was encapsulated within the exosomes. CRISPR-transfected (Id1 knockout) FLS showed a 75% decrease in cell proliferation compared to sham-transfected cells. Lastly, IDB analysis showed robust signals against citId1 from multiple RA PB sera and SFs. Our data show that Id1 is not only an important nuclear protein but is released from FLS, primarily in exosomes, expanding its role in the orchestration of inflammatory lesions through trans-cellular effects. We also show for the first time the presence of ACPAs with specificity to citId1 in RA PB sera and SFs and propose citId1 as a novel autoantigen in RA." @default.
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- W4313356570 date "2016-05-01" @default.
- W4313356570 modified "2023-09-28" @default.
- W4313356570 title "Evidence for citrullinated inhibitor of DNA binding 1 as a novel autoantigen in rheumatoid arthritis" @default.
- W4313356570 doi "https://doi.org/10.4049/jimmunol.196.supp.188.12" @default.
- W4313356570 hasPublicationYear "2016" @default.
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