Regulatory T-cell suppressor program co-opts transcription factor IRF4 to control TH2 responses
By Ye Zheng, A. Chaudhry, A. Kas, Paul C. Deroos, J. Kim, Tin-Tin Chu, L. Corcoran, P. Treuting, U. Klein, Alexander Y. Rudensky. Nature, 2009
613 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/c81560dc143a011d1030148679d6d21456e2bf43
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
- Naganari Ohkura
- Dan R. Littman
- Shimon Sakaguchi
- M. Chong
- Y. Kitagawa
- Liang Zhou
- T. Malek
- Alexander Y. Rudensky
Citations in the corpus
- Transcriptional control of adipose lipid handling by IRF4 (2011, neutral): “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).”
- CD4+T Cells: Differentiation and Functions (2012, background): “IRF4 inactivation in Foxp3+ cells resulted in Th2 development and increased germinal centre formation [113].”
- Plasticity of CD4+ T cell lineage differentiation. (2009, background): “Irf4 was also identified as a direct target of Foxp3, and its selective loss in Treg cells selectively impaired suppression of Th2 cell responses (Zheng et al., 2009).”
- Differentiation of Effector CD4 T Cell Populations (2010, neutral): “Mice with a conditional Irf4 deletion in Tregs may develop Th2-like diseases, although the number of Foxp3+ cells in these mice appears to be normal (37).”
- Development and maintenance of regulatory T cells. (2013, background): “Treg-cell-specific deletion of Irf4 prevents Treg cells from efficiently suppressing Th2 immune responses, leading to uncontrolled Th2 immune responses (Zheng et al., 2009).”
- Interleukin-10 signaling in regulatory T cells is required for suppression of Th17 cell-mediated inflammation (2011, neutral): “In support of this notion, in Treg cells, expression of T-bet and IRF-4 (transcription factors involved in Th1 and Th2 cell differentiation, respectively) facilitates Treg cell-mediated suppression of the corresponding type of response (Koch et al., 2009; Zheng et al., 2009).”