The many faces of Th17 cells

被引:190
作者
Peters, Anneli [1 ]
Lee, Youjin [1 ]
Kuchroo, Vijay K. [1 ]
机构
[1] Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA
关键词
GROWTH-FACTOR-BETA; T-CELLS; TGF-BETA; CUTTING EDGE; T(H)17 DIFFERENTIATION; RECEPTOR; CYTOKINE; IL-21; INFLAMMATION; DRIVES;
D O I
10.1016/j.coi.2011.08.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Th17 cells have been shown to be strong inducers of tissue inflammation and autoimmune diseases. However, not all Th17 cells are pathogenic and increasing data suggest that Th17 cells may come in different flavors. Thus, Th17 cells cannot be described using a narrow schematic, but instead Th17 cells comprise a wide spectrum with a range of effector phenotypes. Here, we review the key factors that generate such diversity, as well as the cytokines and transcription factors that are differentially expressed in pathogenic and nonpathogenic Th17 cells. This new knowledge can be used to identify molecules that make Th17 cells pathogenic and determine how these cells could be targeted to suppress autoimmune diseases.
引用
收藏
页码:702 / 706
页数:5
相关论文
共 50 条
[1]   Encephalitogenic T cells that stably express both T-bet and RORγt consistently produce IFNγ but have a spectrum of IL-17 profiles [J].
Abromson-Leeman, Sara ;
Bronson, Roderick T. ;
Dorf, Martin E. .
JOURNAL OF NEUROIMMUNOLOGY, 2009, 215 (1-2) :10-24
[2]   Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17-producing human T helper cells [J].
Acosta-Rodriguez, Eva V. ;
Napolitani, Giorgio ;
Lanzavecchia, Antonio ;
Sallusto, Federica .
NATURE IMMUNOLOGY, 2007, 8 (09) :942-949
[3]   Interleukin-23 Drives Intestinal Inflammation through Direct Activity on T Cells [J].
Ahern, Philip P. ;
Schiering, Chris ;
Buonocore, Sofia ;
McGeachy, Mandy J. ;
Cua, Dan J. ;
Maloy, Kevin J. ;
Powrie, Fiona .
IMMUNITY, 2010, 33 (02) :279-288
[4]   Cutting Edge: IL-23 Receptor GFP Reporter Mice Reveal Distinct Populations of IL-17-Producing Cells [J].
Awasthi, Amit ;
Riol-Blanco, Lorena ;
Jaeger, Anneli ;
Korn, Thomas ;
Pot, Caroline ;
Galileos, George ;
Bettelli, Estelle ;
Kuchroo, Vijay K. ;
Oukka, Mohamed .
JOURNAL OF IMMUNOLOGY, 2009, 182 (10) :5904-5908
[5]   Highly purified Th17 cells from BDC2.5NOD mice convert into Th1-like cells in NOD/SCID recipient mice [J].
Bending, David ;
De La Pena, Hugo ;
Veldhoen, Marc ;
Phillips, Jenny M. ;
Uyttenhove, Catherine ;
Stockinger, Brigitta ;
Cooke, Anne .
JOURNAL OF CLINICAL INVESTIGATION, 2009, 119 (03) :565-572
[6]   Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis [J].
Bettelli, E ;
Sullivan, B ;
Szabo, SJ ;
Sobel, RA ;
Glimcher, H ;
Kuchroo, VK .
JOURNAL OF EXPERIMENTAL MEDICINE, 2004, 200 (01) :79-87
[7]   Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells [J].
Bettelli, E ;
Carrier, YJ ;
Gao, WD ;
Korn, T ;
Strom, TB ;
Oukka, M ;
Weiner, HL ;
Kuchroo, VK .
NATURE, 2006, 441 (7090) :235-238
[8]   Interleukin-10 Signaling in Regulatory T Cells Is Required for Suppression of Th17 Cell-Mediated Inflammation [J].
Chaudhry, Ashutosh ;
Samstein, Robert M. ;
Treuting, Piper ;
Liang, Yuqiong ;
Pils, Marina C. ;
Heinrich, Jan-Michael ;
Jack, Robert S. ;
Wunderlich, F. Thomas ;
Bruening, Jens C. ;
Mueller, Werner ;
Rudensky, Alexander Y. .
IMMUNITY, 2011, 34 (04) :566-578
[9]   RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation [J].
Codarri, Laura ;
Gyuelveszi, Gabor ;
Tosevski, Vinko ;
Hesske, Lysann ;
Fontana, Adriano ;
Magnenat, Laurent ;
Suter, Tobias ;
Becher, Burkhard .
NATURE IMMUNOLOGY, 2011, 12 (06) :560-U248
[10]   Cutting edge: IL-21 is not essential for Th17 differentiation or experimental autoimmune encephalomyelitis [J].
Coquet, Jonathan M. ;
Chakravarti, Sumone ;
Smyth, Mark J. ;
Godfrey, Dale I. .
JOURNAL OF IMMUNOLOGY, 2008, 180 (11) :7097-7101