IL-17 targeted therapies for psoriasis

被引:136
作者
Chiricozzi, Andrea [1 ]
Krueger, James G. [1 ,2 ,3 ]
机构
[1] Rockefeller Univ, Lab Invest Dermatol, New York, NY 10065 USA
[2] Rockefeller Univ, Milstein Med Res Program, New York, NY 10065 USA
[3] Rockefeller Univ, New York, NY 10065 USA
关键词
anti-IL-17; agents; brodalumab; IL-17; ixekizumab; psoriasis; secukinumab; T-CELL POPULATION; DENDRITIC CELLS; AUTOIMMUNE INFLAMMATION; HUMAN SKIN; EPIDERMAL HYPERPLASIA; MONOCLONAL-ANTIBODY; PLAQUE PSORIASIS; CYTOKINE FAMILY; INTERLEUKIN; 22; HELPER TYPE-1;
D O I
10.1517/13543784.2013.806483
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Introduction: Psoriasis is a chronic, disabling, inflammatory skin disease whose pathogenesis still remains to be fully elucidated. Genetic and environmental factors induce an immune response mediated by several cytokines and chemokines, including IL-17A. Areas covered: Emerging evidence now suggests that IL-17A is central in the pathogenesis of psoriasis. Three agents neutralizing IL-17 (i.e., secukinumab and ixekizumab) or antagonizing its receptor (i.e., brodalumab) are in development and are being studied in Phase III clinical trials to evaluate their overall efficacy and safety. However, Phase II results of IL-17 blockade with each of these agents has shown a marked improvement of disease severity, thus confirming the pathogenic relevance of IL-17 in mediating crucial inflammatory circuits in psoriasis. Expert opinion: Anti-IL-17 agents are likely to become important future therapeutics in this disease and the may potentially impact on cardiovascular diseases, arthritis and other comorbidities associated with psoriasis.
引用
收藏
页码:993 / 1005
页数:13
相关论文
共 99 条
[1]   Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17 [J].
Aggarwal, S ;
Ghilardi, N ;
Xie, MH ;
de Sauvage, FJ ;
Gurney, AL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (03) :1910-1914
[2]   Resident skin cells in psoriasis:: a special took at the pathogenetic functions of keratinocytes [J].
Albanesi, Cristina ;
De Pita, Ornella ;
Girolomoni, Giampiero .
CLINICS IN DERMATOLOGY, 2007, 25 (06) :581-588
[3]   Induction and effector functions of TH17 cells [J].
Bettelli, Estelle ;
Korn, Thomas ;
Oukka, Mohamed ;
Kuchroo, Vijay K. .
NATURE, 2008, 453 (7198) :1051-1057
[4]   Psoriasis patients show signs of insulin resistance [J].
Boehncke, S. ;
Thaci, D. ;
Beschmann, H. ;
Ludwig, R. J. ;
Ackermann, H. ;
Badenhoop, K. ;
Boehncke, W-H. .
BRITISH JOURNAL OF DERMATOLOGY, 2007, 157 (06) :1249-1251
[5]   Psoriasis - a systemic inflammatory disorder: clinic, pathogenesis and therapeutic perspectives [J].
Boehncke, Wolf-Henning ;
Sterry, Wolfram .
JOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT, 2009, 7 (11) :946-952
[6]   Health economics and the modern management of psoriasis [J].
Burden, A. D. .
BRITISH JOURNAL OF DERMATOLOGY, 2010, 163 (04) :670-671
[7]  
Cai YH, 2011, IMMUNITY, V35, P596, DOI 10.1016/j.immuni.2011.08.001
[8]   IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis [J].
Chan, Jason R. ;
Blumenschein, Wendy ;
Murphy, Erin ;
Diveu, Caroline ;
Wiekowski, Maria ;
Abbondanzo, Susan ;
Lucian, Linda ;
Geissler, Richard ;
Brodie, Scott ;
Kimball, Alexa B. ;
Gorman, Daniel M. ;
Smith, Kathleen ;
Malefyt, Rene de Waal ;
Kastelein, Robert A. ;
McClanahan, Terrill K. ;
Bowman, Edward P. .
JOURNAL OF EXPERIMENTAL MEDICINE, 2006, 203 (12) :2577-2587
[9]   Anti-IL-17A therapy protects against bone erosion in experimental models of rheumatoid arthritis [J].
Chao, Cheng-Chi ;
Chen, Shi-Juan ;
Adamopoulos, Iannis E. ;
Davis, Nicole ;
Hong, Kyu ;
Vu, Anna ;
Kwan, Sylvia ;
Fayadat-Dilman, Laurence ;
Asio, Agelio ;
Bowman, Edward P. .
AUTOIMMUNITY, 2011, 44 (03) :243-252
[10]   Emerging Role of IL-17 in Atherosclerosis [J].
Chen, Shuang ;
Crother, Timothy R. ;
Arditi, Moshe .
JOURNAL OF INNATE IMMUNITY, 2010, 2 (04) :325-333