Th17 cells: A new paradigm for cutaneous inflammation

被引:33
作者
Asarch, Adam [1 ]
Barak, Orr [1 ]
Loo, Daniel S. [1 ]
Gottlieb, Alice B. [1 ]
机构
[1] Tufts Univ, Med Ctr, Dept Dermatol, Boston, MA 02111 USA
关键词
autoimmune disease; cutaneous immunology; cutaneous inflammation; IL-17; IL-22; IL-23; psoriasis; Th17; cells;
D O I
10.1080/09546630802206686
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Inflammatory processes of the skin have classically been segregated to either the cell-mediated, T-helper type 1 (Th1) or the humoral (Th2) branch of the immune system. The recent addition of Th17 cells, a novel T-helper cell named for its secretion of interleukin (IL)-17, to current thinking in autoimmunity has resulted in a significant paradigm shift in immunological thinking. Collectively, Th17 cytokines have been found to stimulate cutaneous immune reactions through an activation of a wide range of downstream inflammatory mediators and an induction of immune cell and keratinocyte proliferation as well as angiogenesis. Newly developed treatment modalities for neutralizing the Th17 branch of the immune system are proving to be valuable additions to the current therapeutic armamentarium. Here we describe a new schema for dermatologic T-cell-mediated immunity. We elucidate experiments confirming the presence of Th17 cells, followed by a discussion of their relevance to cutaneous inflammation and psoriasis.
引用
收藏
页码:259 / 266
页数:8
相关论文
共 89 条
[41]   Latent TGFβ1 overexpression in keratinocytes results in a severe psoriasis-like skin disorder [J].
Li, AG ;
Wang, D ;
Feng, XH ;
Wang, XJ .
EMBO JOURNAL, 2004, 23 (08) :1770-1781
[42]   Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides [J].
Liang, Spencer C. ;
Tan, Xiang-Yang ;
Luxenberg, Deborah P. ;
Karim, Riyez ;
Dunussi-Joannopoulos, Kyriaki ;
Collins, Mary ;
Fouser, Lynette A. .
JOURNAL OF EXPERIMENTAL MEDICINE, 2006, 203 (10) :2271-2279
[43]   IL-22 is required for Th17 cell-mediated pathology in a mouse model of psoriasis-like skin inflammation [J].
Ma, Hak-Ling ;
Liang, Spencer ;
Li, Jing ;
Napierata, Lee ;
Brown, Tom ;
Benoit, Stephen ;
Senices, Mayra ;
Gill, Davinder ;
Dunussi-Joannopoulos, Kyriaki ;
Collins, Mary ;
Nickerson-Nutter, Cheryl ;
Fouser, Lynette A. ;
Young, Deborah A. .
JOURNAL OF CLINICAL INVESTIGATION, 2008, 118 (02) :597-607
[44]   Transforming growth factor-β induces development of the TH17 lineage [J].
Mangan, PR ;
Harrington, LE ;
O'Quinn, DB ;
Helms, WS ;
Bullard, DC ;
Elson, CO ;
Hatton, RD ;
Wahl, SM ;
Schoeb, TR ;
Weaver, CT .
NATURE, 2006, 441 (7090) :231-234
[45]  
Matusevicius D, 1999, MULT SCLER J, V5, P101, DOI 10.1177/135245859900500206
[46]   T cells doing it for themselves:: TGF-β regulation of Th1 and Th17 cells [J].
McGeachy, Mandy J. ;
Cua, Daniel J. .
IMMUNITY, 2007, 26 (05) :547-549
[47]   The IL23 axis plays a key role in the pathogenesis of IBD [J].
McGovern, Dermot ;
Powrie, Fiona .
GUT, 2007, 56 (10) :1333-1336
[48]  
McInnes IB, 2006, E SCHERING RES FDN W, V56, P29
[49]   Interleukin-15: a new cytokine target for the treatment of inflammatory diseases [J].
McInnes, IB ;
Gracie, JA .
CURRENT OPINION IN PHARMACOLOGY, 2004, 4 (04) :392-397
[50]   Understanding the IL-23-IL-17 immune pathway [J].
McKenzie, BS ;
Kastelein, RA ;
Cua, DJ .
TRENDS IN IMMUNOLOGY, 2006, 27 (01) :17-23