<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Miura Y</submitter><funding>grants-in-aid from the Ministry of Education, Culture, Sports, Science and Technology (MEXT)/JSPS KAKENHI</funding><funding>Bristol-Myers Squibb K.K. and Ono Pharmaceutical Co., LTD</funding><pagination>16363</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9525600</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(1)</volume><pubmed_abstract>CD80 interact with CD28 and CTLA-4 on antigen-presenting cells, and function in the co-stimulatory signaling that regulates T cell activity. CTLA-4-Ig is used to treat RA by blocking co-stimulatory signaling. Chronic inflammatory arthritis was induced in D1BC mice using low-dose arthritogenic antigens and treated with CTLA-4-Ig. We performed histopathology of the joints and lymph nodes, serological examination for rheumatoid factors, and flow cytometric analysis of isolated synovial cells, including CD45&lt;sup>-&lt;/sup> FLSs and CD45&lt;sup>+&lt;/sup> synovial macrophages. CTLA-4-Ig treatment ameliorated the chronic inflammatory polyarthritis. There was a decrease in the number of infiltrating lymphoid cells in the joints as well as in the levels of RF-IgG associated with a decrease in the number of</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>CTLA-4-Ig internalizes CD80 in fibroblast-like synoviocytes from chronic inflammatory arthritis mouse model.</pubmed_title><pmcid>PMC9525600</pmcid><funding_grant_id>JP 20K17447</funding_grant_id><funding_grant_id>JP 26461470</funding_grant_id><pubmed_authors>Kanazawa S</pubmed_authors><pubmed_authors>Miura Y</pubmed_authors><pubmed_authors>Maeda S</pubmed_authors><pubmed_authors>Isogai S</pubmed_authors></additional><is_claimable>false</is_claimable><name>CTLA-4-Ig internalizes CD80 in fibroblast-like synoviocytes from chronic inflammatory arthritis mouse model.</name><description>CD80 interact with CD28 and CTLA-4 on antigen-presenting cells, and function in the co-stimulatory signaling that regulates T cell activity. CTLA-4-Ig is used to treat RA by blocking co-stimulatory signaling. Chronic inflammatory arthritis was induced in D1BC mice using low-dose arthritogenic antigens and treated with CTLA-4-Ig. We performed histopathology of the joints and lymph nodes, serological examination for rheumatoid factors, and flow cytometric analysis of isolated synovial cells, including CD45&lt;sup>-&lt;/sup> FLSs and CD45&lt;sup>+&lt;/sup> synovial macrophages. CTLA-4-Ig treatment ameliorated the chronic inflammatory polyarthritis. There was a decrease in the number of infiltrating lymphoid cells in the joints as well as in the levels of RF-IgG associated with a decrease in the number of</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2026-07-14T15:49:49.383Z</modification><creation>2025-02-19T00:23:47.616Z</creation></dates><accession>S-EPMC9525600</accession><cross_references><pubmed>36180526</pubmed><doi>10.1038/s41598-022-20694-7</doi></cross_references></HashMap>