{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T07:00:45Z","timestamp":1791529245419,"version":"4.3.4"},"reference-count":25,"publisher":"Springer Science and Business Media LLC","issue":"5","license":[{"start":{"date-parts":[[2021,12,2]],"date-time":"2021-12-02T00:00:00Z","timestamp":1638403200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2021,12,2]],"date-time":"2021-12-02T00:00:00Z","timestamp":1638403200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Ir J Med Sci"],"published-print":{"date-parts":[[2022,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                <jats:title>Background<\/jats:title>\n                <jats:p>Cell division control protein 42 (CDC42) is reported to be involved in multiple inflammation processes by regulating T cell differentiation, maintaining immune cell homeostasis, and altering their function, while no relevant studies explored its clinical role in patients with rheumatoid arthritis (RA). Therefore, this study aimed to explore the correlation of CDC42 with Th1 and Th17 cells and its association with disease risk, activity, and treatment outcomes of RA.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>After the enrollment of 95 active RA patients and 50 healthy subjects (HC), their CDC42, Th1 cells, and Th17 cells were assayed by RT-qPCR and flow cytometry, accordingly. For RA patients only, CDC42 was also detected at W6, and W12 after treatment. The treatment response and remission status were evaluated at W12.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Compared to HC, CDC42 was reduced (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001), while Th1 cells (<jats:italic>P<\/jats:italic>\u2009=\u20090.021) and Th17 cells (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) were increased in RA patients. Besides, CDC42 was negatively correlated with Th17 cells (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001), erythrocyte sedimentation rate (ESR) (<jats:italic>P<\/jats:italic>\u2009=\u20090.012), C-reactive protein (<jats:italic>P<\/jats:italic>\u2009=\u20090.002), and disease activity score in 28 joints (DAS28) (<jats:italic>P<\/jats:italic>\u2009=\u20090.007), but did not relate to Th1 cells or other disease features (all <jats:italic>P<\/jats:italic>\u2009&gt;\u20090.05) in RA patients. Furthermore, CDC42 was elevated during treatment in RA patients (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001). Moreover, CDC42 increment at W12 correlated with treatment response (<jats:italic>P<\/jats:italic>\u2009=\u20090.004). Besides, CDC42 elevation at W0 (<jats:italic>P<\/jats:italic>\u2009=\u20090.038), W6 (<jats:italic>P<\/jats:italic>\u2009=\u20090.001), and W12 (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) also linked with treatment remission.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>CDC42 has the potential to serve as a biomarker to monitor disease activity and treatment efficacy in patients with RA.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s11845-021-02858-y","type":"journal-article","created":{"date-parts":[[2021,12,2]],"date-time":"2021-12-02T18:03:44Z","timestamp":1638468224000},"page":"2155-2161","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["The relationship of blood CDC42 level with Th1 cells, Th17 cells, inflammation markers, disease risk\/activity, and treatment efficacy of rheumatoid arthritis"],"prefix":"10.1007","volume":"191","author":[{"given":"Yongji","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wendi","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3227-6864","authenticated-orcid":false,"given":"Feng","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,12,2]]},"reference":[{"issue":"10055","key":"2858_CR1","doi-asserted-by":"publisher","first-page":"2023","DOI":"10.1016\/S0140-6736(16)30173-8","volume":"388","author":"JS Smolen","year":"2016","unstructured":"Smolen JS, Aletaha D, McInnes IB (2016) Rheumatoid arthritis. 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And the written informed consents were obtained from all subjects.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"The authors declare no competing interests.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Conflict of interest"}}]}}