The development of inflammatory TH-17 cells requires interferon-regulatory factor 4

By A. Brüstle, Sylvia Heink, M. Huber, Christine Rosenplänter, C. Stadelmann, P. Yu, E. Arpaia, T. Mak, T. Kamradt, M. Lohoff. Nature Immunology, 2007

710 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/fb35791e38923ba8c59481c9a3a80998c59b4fce

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Citations in the corpus

• Plasticity of CD4+ T cell lineage differentiation. (2009, background): “IRF4 is essential for Th17 cell differentiation both in vitro and in vivo (Brustle et al., 2007).”
• IL-17 and Th17 Cells. (2009, background): “Consistent with this observation, IRF4deficient T cells failed to upregulate RORγt upon stimulation in the presence of TGFβ plus IL-6 and could not be differentiated into Th17 cells (63).”
• Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis (2010, background): “Th17 cell differentiation is associated with expression of several transcription factors, including RORgt, RORa, RUNX1, BATF, IRF-4, AHR, and c-Maf (Bauquet et al., 2009; Brüstle et al., 2007; Ivanov et al., 2006; Schraml et al., 2009; Veldhoen et al., 2008; Yang et al., 2008b; Zhang et al., 2008).”
• Transcriptional control of adipose lipid handling by IRF4 (2011, positive): “IRF4 is a well-known participant in a variety of immune activities, including regulatory T cell function and the development of inflammatory T(H)-17 cells, as well as plasma cell differentiation (Brustle et al., 2007; Klein et al., 2006; Mittrucker et al., 1997; Zheng et al., 2009).”
• Retinoid-related orphan receptors (RORs): critical roles in development, immunity, circadian rhythm, and cellular metabolism (2009, background): “In addition to the STAT transcription factors, interferon regulatory factor 4 (IRF4) has been reported to regulate T lineage commitment and to be required for Th17 differentiation [Brustle et al., 2007; Huber et al., 2008].”
• Critical regulation of early Th17 cell differentiation by IL-1 signaling (2009, background): “IL-1 Signaling in T Cells Is Necessary for Th17 Responses In Vivo IL-1R1 is necessary for the induction of EAE disease in mice (Brustle et al., 2007), which could be a result of defective IL-1 signaling in Immunity 30, 576–587, April 17, 2009 a2009 Elsevier Inc.”
• CD4+T Cells: Differentiation and Functions (2012, background): “Irf4(−/−)mice failed to enhance expression of RORγt and subsequently did not develop experimental autoimmune encephalitis as a result of impaired Th17 response [75].”