Rheumatoid arthritis: developing pharmacological therapies

被引:21
作者
Abbott, JD [1 ]
Moreland, LW [1 ]
机构
[1] Univ Alabama Birmingham, Dept Med, Div Clin Immunol & Rheumatol, Birmingham, AL 35294 USA
关键词
abatcept; biological response modifiers; CTLA4; immunoglobulin; IL-1; IL-6; IL-15; IL-18; MRA; rheumatoid arthritis; rituximab; TNF-alpha; TNF inhibitors;
D O I
10.1517/13543784.13.8.1007
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Rheumatoid arthritis (RA) is a chronic inflammatory disease that often results in significant morbidity, mortality and disability. Over the past 20 years a better understanding of the pathogenesis of RA has led to the development of new approaches to disease treatment. The recent introduction of biological agents has changed the treatment paradigm for RA. The success of early biological therapies including TNF-alpha and IL-1 antagonists has spurred interest in the development of additional novel targets in the treatment of RA. Biological therapies approved for other indications, such as rituximab, are now being evaluated for the treatment of rheumatic diseases such as RA. A costimulatory blocker, abatacept, is also in pivotal Phase III trials. This article reviews evolving pharmacological therapies in RA with an emphasis on the newer approaches to treatment including inhibition of cognate signalling and T- and B-cell targets.
引用
收藏
页码:1007 / 1018
页数:12
相关论文
共 77 条
[1]   CTLA4Ig-mediated blockade of T-cell costimulation in patients with psoriasis vulgaris [J].
Abrams, JR ;
Lebwohl, MG ;
Guzzo, CA ;
Jegasothy, BV ;
Goldfarb, MT ;
Goffe, BS ;
Menter, A ;
Lowe, NJ ;
Krueger, G ;
Brown, MJ ;
Weiner, RS ;
Birkhofer, MJ ;
Warner, GL ;
Berry, KK ;
Linsley, PS ;
Krueger, JG ;
Ochs, HD ;
Kelley, SL ;
Kang, SW .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (09) :1243-1252
[2]   Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plaques, including the activation of keratinocytes, dendritic cells, and endothelial cells [J].
Abrams, JR ;
Kelley, SL ;
Hayes, E ;
Kikuchi, T ;
Brown, MJ ;
Kang, SW ;
Lebwohl, MG ;
Guzzo, CA ;
Jegasothy, BV ;
Linsley, PS ;
Krueger, JG .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 192 (05) :681-693
[3]  
BASLUND B, 2003, AM COLL RHEUM 67 ANN
[4]   Interleukin 6 knock-out mice are resistant to antigen-induced experimental arthritis [J].
Boe, A ;
Baiocchi, M ;
Carbonatto, M ;
Papoian, R ;
Serlupi-Crescenzi, O .
CYTOKINE, 1999, 11 (12) :1057-1064
[5]  
Bresnihan B, 1998, ARTHRITIS RHEUM, V41, P2196, DOI 10.1002/1529-0131(199812)41:12<2196::AID-ART15>3.0.CO
[6]  
2-2
[7]   Effects of a PEGylated soluble TNF receptor type 1 (PEG sTNF-RI) on cytokine expression in adjuvant arthritis [J].
Bush, KA ;
Walker, JS ;
Frazier, J ;
Kirkham, BW .
SCANDINAVIAN JOURNAL OF RHEUMATOLOGY, 2002, 31 (04) :198-204
[8]   Serologic changes following B lymphocyte depletion therapy for rheumatoid arthritis [J].
Cambridge, G ;
Leandro, MJ ;
Edwards, JCW ;
Ehrenstein, MR ;
Salden, M ;
Bodman-Smith, M ;
Webster, ADB .
ARTHRITIS AND RHEUMATISM, 2003, 48 (08) :2146-2154
[9]  
Choy E, 2003, ANN RHEUM DIS, V62, P68
[10]   Efficacy of a novel PEGylated humanized anti-TNF fragment (CDP870) in patients with rheumatoid arthritis: a phase II double-blinded, randomized, dose-escalating trial [J].
Choy, EHS ;
Hazleman, B ;
Smith, M ;
Moss, K ;
Lisi, L ;
Scott, DGI ;
Patel, J ;
Sopwith, M ;
Isenberg, DA .
RHEUMATOLOGY, 2002, 41 (10) :1133-1137