{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T16:25:33Z","timestamp":1792686333859,"version":"4.5.0"},"reference-count":49,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2024,5,8]],"date-time":"2024-05-08T00:00:00Z","timestamp":1715126400000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Int J of Rheum Dis"],"published-print":{"date-parts":[[2024,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objectives<\/jats:title><jats:p>This study investigates the role of TNF\u2010induced protein 3 (TNFAIP3) and CCAAT\/enhancer\u2010binding protein \u03b2 (C\/EBP\u03b2) in alveolar macrophages (AMs) of patients with systemic sclerosis\u2010associated interstitial lung disease (SSc\u2010ILD) and their influence on pulmonary fibrosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Transfection of HEK293T cells and AMs with plasmids carrying TNFAIP3 and C\/EBP\u03b2 was performed, followed by co\u2010culturing AMs with pulmonary fibroblasts. Immunoblotting analysis was then utilized to assess the expression of TNFAIP3, C\/EBP\u03b2, and collagen type 1 (Col1). Quantitative PCR analysis was conducted to quantify the mRNA levels of <jats:italic>C\/EBP\u03b2<\/jats:italic>, <jats:italic>IL\u201010<\/jats:italic>, and <jats:italic>TGF\u2010\u03b21<\/jats:italic>. STRING database analysis, and immunoprecipitation assays were employed to investigate the interactions between TNFAIP3 and C\/EBP\u03b2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>TNFAIP3 expression was significantly reduced in SSc\u2010ILD AMs, correlating with increased Col1 production in fibroblasts. Overexpression of TNFAIP3 inhibited this pro\u2010fibrotic activity. Conversely, C\/EBP\u03b2 expression was elevated in SSc\u2010ILD AMs, and its reduction through TNFAIP3 restoration decreased pro\u2010fibrotic cytokines IL\u201010 and TGF\u03b21 levels. Protein\u2013protein interaction studies confirmed the regulatory relationship between TNFAIP3 and C\/EBP\u03b2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>This study highlights the important role of TNFAIP3 in regulating pulmonary fibrosis in SSc\u2010ILD by modulating C\/EBP\u03b2 expression in AMs. These findings suggest that targeting TNFAIP3 could be a potential therapeutic strategy for managing SSc\u2010ILD patients.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1756-185x.15174","type":"journal-article","created":{"date-parts":[[2024,5,9]],"date-time":"2024-05-09T04:54:56Z","timestamp":1715230496000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Dysregulation of TNF\u2010induced protein 3 and CCAAT\/enhancer\u2010binding protein \u03b2 in alveolar macrophages: Implications for systemic sclerosis\u2010associated interstitial lung 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