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000279433 1001_ $$0P:(DE-2719)2812698$$aKöhne, Maren$$b0$$udzne
000279433 245__ $$aSatb1 directs the differentiation of TH17 cells through suppression of IL-2 expression.
000279433 260__ $$aMaryland Heights, MO$$bCell Press$$c2025
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000279433 520__ $$aT helper (TH)17 cells are crucial for host defense in barrier organs, and their altered functionality can disrupt tissue homeostasis, increasing the risk of autoimmune diseases. Thus, it is essential to understand the mechanisms controlling TH17 differentiation to develop strategies influencing their role in diseases. Here, we identified Special AT-rich sequence-binding protein 1 (Satb1) as a pioneering factor for TH17 development. Satb1 is highly expressed in TH17 cells, and loss of Satb1 prevents the differentiation of TH17 cells. Consequently, expression of Satb1 in CD4+ T cells is required for the formation of TH17-driven autoimmune diseases. Mechanistically, Satb1 mediates TH17 development through regulating accessibility of the Il2 gene locus and thereby preventing interleukin (IL)-2 signaling early during TH17 differentiation. Hence, suppression of IL-2 expression by Satb1 during TH17 formation is pivotal, suggesting that Satb1 could serve as a novel therapeutic target for treating autoimmune diseases driven by TH17 cells.
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000279433 650_7 $$2Other$$aCD4(+) T cell differentiation
000279433 650_7 $$2Other$$aCP: Immunology
000279433 650_7 $$2Other$$aEAE
000279433 650_7 $$2Other$$aIL-2
000279433 650_7 $$2Other$$aSatb1
000279433 650_7 $$2Other$$aT(H)17 cells
000279433 650_7 $$2Other$$aautoimmune disease
000279433 650_7 $$2Other$$acolitis
000279433 650_7 $$2Other$$ascRNA-seq
000279433 650_7 $$2Other$$asingle-cell MultiOMICs
000279433 7001_ $$0P:(DE-2719)2814240$$aShakiba, Mehrnoush Hadaddzadeh$$b1$$udzne
000279433 7001_ $$0P:(DE-2719)2812337$$aSchmidleithner, Lisa$$b2
000279433 7001_ $$0P:(DE-2719)9001500$$aSchulte-Schrepping, Jonas$$b3$$udzne
000279433 7001_ $$0P:(DE-2719)9001595$$aScholz, Rebekka$$b4$$udzne
000279433 7001_ $$0P:(DE-2719)9000539$$aElmzzahi, Tarek$$b5$$udzne
000279433 7001_ $$0P:(DE-HGF)0$$aSommer, Daniel$$b6
000279433 7001_ $$0P:(DE-2719)9001790$$aLi, Yuanfang$$b7$$udzne
000279433 7001_ $$0P:(DE-2719)9001303$$aCarraro, Caterina$$b8$$udzne
000279433 7001_ $$0P:(DE-2719)9000846$$aDe Domenico, Elena$$b9$$udzne
000279433 7001_ $$0P:(DE-HGF)0$$aWißfeld, Jannis$$b10
000279433 7001_ $$0P:(DE-2719)2812735$$aHändler, Kristian$$b11$$udzne
000279433 7001_ $$0P:(DE-2719)9000568$$aHamada, Doaa$$b12$$udzne
000279433 7001_ $$0P:(DE-2719)9002087$$aFrolov, Aleksej$$b13$$udzne
000279433 7001_ $$0P:(DE-2719)9002527$$aCheng, Xiaoxiao$$b14$$udzne
000279433 7001_ $$0P:(DE-HGF)0$$aBaumgart, Ann-Kathrin$$b15
000279433 7001_ $$0P:(DE-2719)9001067$$aHolsten, Lisa$$b16$$udzne
000279433 7001_ $$0P:(DE-2719)2813660$$aOsei-Sarpong, Collins$$b17$$udzne
000279433 7001_ $$0P:(DE-2719)2811740$$aBourry, Svenja$$b18
000279433 7001_ $$aThabet, Yasser$$b19
000279433 7001_ $$0P:(DE-HGF)0$$aRenken, Hannes$$b20
000279433 7001_ $$0P:(DE-2719)9002116$$aPaulusch, Stefan$$b21$$udzne
000279433 7001_ $$aSadlon, Timothy$$b22
000279433 7001_ $$aBuch, Thorsten$$b23
000279433 7001_ $$aWunderlich, F Thomas$$b24
000279433 7001_ $$aWickenhauser, Claudia$$b25
000279433 7001_ $$aAlferink, Judith$$b26
000279433 7001_ $$aKuhlmann, Tanja$$b27
000279433 7001_ $$aGeyer, Matthias$$b28
000279433 7001_ $$0P:(DE-2719)9001512$$aBonaguro, Lorenzo$$b29$$udzne
000279433 7001_ $$aBarry, Simon C$$b30
000279433 7001_ $$0P:(DE-2719)2811660$$aSchultze, Joachim L$$b31$$udzne
000279433 7001_ $$0P:(DE-2719)2812219$$aBeyer, Marc D$$b32$$eLast author$$udzne
000279433 773__ $$0PERI:(DE-600)2649101-1$$a10.1016/j.celrep.2025.115866$$gVol. 44, no. 7, p. 115866 -$$n7$$p115866$$tCell reports$$v44$$x2211-1247$$y2025
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