Please use this identifier to cite or link to this item:
Title: Egr2 and 3 control adaptive immune responses by temporally uncoupling expansion from T cell differentiation
Authors: Li, S
Li, SL
Issue Date: 2017
Publisher: Rockefeller University Press
Citation: Journal of Experimental Medicine, (2017)
Abstract: Egr2 and 3 are important for maintaining immune homeostasis. Here we define a fundamental function of Egr2 and 3 operating as a checkpoint that controls the transition between clonal expansion and differentiation of effector T cells. Egr2 and 3 deficiency resulted in defective clonal expansion, but hyper-activation and excessive differentiation of T cells in response to viral infection. Conversely, sustained Egr2 expression enhanced expansion, but severely impaired effector differentiation. Egr2 bound to and controlled the expression of genes regulating proliferation (Myc, Myb) and differentiation repressors (Bcl6, Id3), while repressing transcription factors required for effector function (Zeb2, RORa, RORc, Bhlhe40). Egr2 and 3 expression in T cells was regulated reciprocally by antigen and IFNγ providing a mechanism for adjusting proliferation and differentiation of individual T cells. Thus, Egr2 and 3 are upstream regulators of effector CD4 and CD8 T cells that are essential for optimal responses with limited immunopathology.
ISSN: 0022-1007
Appears in Collections:Dept of Life Sciences Research Papers

Files in This Item:
File Description SizeFormat 
Fulltext.pdf10.44 MBAdobe PDFView/Open

Items in BURA are protected by copyright, with all rights reserved, unless otherwise indicated.