000111401 001__ 111401
000111401 005__ 20180317092325.0
000111401 0247_ $$2doi$$a10.1016/j.immuni.2007.05.021
000111401 037__ $$aARTICLE
000111401 245__ $$aDirect regulation of Gata3 expression determines the T helper differentiation potential of Notch
000111401 269__ $$a2007
000111401 260__ $$c2007
000111401 336__ $$aJournal Articles
000111401 520__ $$aCD4(+) T helper cells differentiate into T helper 1 (Th1) or Th2 effector lineages, which orchestrate immunity to different types of microbes. Both Th1 and Th2 differentiation can be induced by Notch, but what dictates which of these programs is activated in response to Notch is not known. By using T cell-specific gene ablation of the Notch effector RBP-J or the Notch1 and 2 receptors, we showed here that Notch was required on CD4(+) T cells for physiological Th2 responses to parasite antigens. GATA-3 was necessary for Notch-induced Th2 differentiation, and we identified an upstream Gata3 promoter as a direct target for Notch signaling. Moreover, absence of GATA-3 turned Notch from a Th2 inducer into a powerful inducer of Th1 differentiation. Therefore, Gata3 is a critical element determining inductive Th2 differentiation and limiting Th1 differentiation by Notch
000111401 700__ $$aAmsen, D.
000111401 700__ $$aAntov, A.
000111401 700__ $$aJankovic, D.
000111401 700__ $$aSher, A.
000111401 700__ $$0240231$$aRadtke, F.$$g172749
000111401 700__ $$aSouabni, A.
000111401 700__ $$aBusslinger, M.
000111401 700__ $$aMcCright, B.
000111401 700__ $$aGridley, T.
000111401 700__ $$aFlavell, R. A.
000111401 773__ $$j27$$k1$$q89-99$$tImmunity
000111401 909CO $$ooai:infoscience.tind.io:111401$$particle$$pSV
000111401 909C0 $$0252086$$pUPRAD$$xU11429
000111401 937__ $$aUPRAD-ARTICLE-2007-006
000111401 973__ $$aEPFL$$rREVIEWED$$sPUBLISHED
000111401 980__ $$aARTICLE