Faculty Opinions recommendation of Transforming Growth Factor-β Signaling in Regulatory T Cells Controls T Helper-17 Cells and Tissue-Specific Immune Responses.

Author(s):  
Jay Kolls
Immunity ◽  
2017 ◽  
Vol 46 (4) ◽  
pp. 660-674 ◽  
Author(s):  
Joanne E. Konkel ◽  
Dunfang Zhang ◽  
Peter Zanvit ◽  
Cheryl Chia ◽  
Tamsin Zangarle-Murray ◽  
...  

2010 ◽  
Vol 135 ◽  
pp. S98
Author(s):  
Sebastien Bertin-Maghit ◽  
Brendan O'Sullivan ◽  
Shannoiin Best ◽  
Emily Duggan ◽  
Dimeng Pang ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Masanori Abe ◽  
Yoichi Hiasa ◽  
Morikazu Onji

Many autoimmune diseases are driven by self-reactive T helper (Th) cells. A new population of effector CD4+T cells characterized by the secretion of interleukin (IL)-17, referred to as Th17 cells, has been demonstrated to be phenotypically, functionally, and developmentally distinct from Th1 and Th2 cells. Because the liver is known to be an important source of transforming growth factor-βand IL-6, which are cytokines that are crucial for Th17 differentiation, it is very likely that Th17 cells contribute to liver inflammation and autoimmunity. In contrast, another distinct subset of T cells, regulatory T cells (Treg), downregulate immune responses and play an important role in maintaining self-tolerance. In addition, there is a reciprocal relationship between Th17 cells and Tregs, in development and effector functions, and the balance between Th17 and Treg cells can affect the outcome of immune responses, particularly in autoimmune diseases. In this review, we will focus on the latest investigative findings related to Th17 cells in autoimmune liver disease.


2010 ◽  
Vol 82 (4) ◽  
pp. 698-705 ◽  
Author(s):  
Jenny Mjösberg ◽  
Göran Berg ◽  
Maria C. Jenmalm ◽  
Jan Ernerudh

2014 ◽  
Vol 49 (6) ◽  
pp. 817-826 ◽  
Author(s):  
V. P. B. Parachuru ◽  
D. E. Coates ◽  
T. J. Milne ◽  
H. M. Hussaini ◽  
A. M. Rich ◽  
...  

2009 ◽  
Vol 206 (10) ◽  
pp. 2131-2139 ◽  
Author(s):  
Jens Nolting ◽  
Carolin Daniel ◽  
Sabine Reuter ◽  
Christina Stuelten ◽  
Peng Li ◽  
...  

It has been reported that retinoic acid (RA) enhances regulatory T (T reg) cell conversion by inhibiting the secretion of cytokines that interfere with conversion. This report shows that these conclusions provide a partial explanation at best. First, RA not only interfered with cytokine secretion but also with the ability of these cytokines to inhibit T reg cell conversion of naive T cells. Furthermore, RA enhanced conversion even in the absence of inhibitory cytokines. The latter effect depended on the RA receptor α (RARα) but did not require Smad3, despite the fact that RA enhanced Smad3 expression. The RARα1 isoform was not essential for RA-dependent enhancement of transforming growth factor β–driven conversion, suggesting that conversion can also be mediated by RARα2. Interleukin (IL)-6 strongly reduced RARα expression levels such that a deficiency of the predominant RARα1 isoform leaves too little RARα2 for RA to inhibit the generation of Th17 cells in the presence of IL-6.


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