Literature DB >> 12810200

Antibody therapy for rheumatoid arthritis.

Peter C Taylor1.   

Abstract

High-quality monoclonal antibodies (mAbs) with specificity for relevant disease molecules can now be produced in abundance. Anti-tumour necrosis factor-alpha therapies have set a new standard for symptom control in rheumatoid arthritis, and blockade of tumour necrosis factor has the potential to protect joints from structural damage. Other targets for therapeutic antibodies include the cytokines interleukin (IL)-1, IL-6, IL-8, IL-15, IL-17 and IL-18. In addition, there is preliminary evidence for the clinical efficacy of both keliximab, a mAb targeting the T cell antigen CD4, and rituximab, a chimeric mAb against the B cell antigen CD20 and CTLA4-Ig, which blocks the CD28/B7 interaction. Phase III studies have yet to be undertaken for these novel biological agents, and it is unclear whether any of these agents will have true disease-modifying capabilities.

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Year:  2003        PMID: 12810200     DOI: 10.1016/s1471-4892(03)00032-8

Source DB:  PubMed          Journal:  Curr Opin Pharmacol        ISSN: 1471-4892            Impact factor:   5.547


  12 in total

Review 1.  [Biologicals: a new therapeutic approach for inflammatory diseases].

Authors:  C E Antoni; B Manger
Journal:  Internist (Berl)       Date:  2004-06       Impact factor: 0.743

2.  An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor-dependent signals.

Authors:  Jeffrey J Yu; Matthew J Ruddy; Grace C Wong; Cornelia Sfintescu; Pamela J Baker; Jeffrey B Smith; Richard T Evans; Sarah L Gaffen
Journal:  Blood       Date:  2007-01-03       Impact factor: 22.113

3.  The case of tumour necrosis factor-alpha inhibitors in the treatment of rheumatoid arthritis: a budget impact analysis.

Authors:  Jan Sørensen; Lis S Andersen
Journal:  Pharmacoeconomics       Date:  2005       Impact factor: 4.981

4.  CD28 delivers a unique signal leading to the selective recruitment of RelA and p52 NF-kappaB subunits on IL-8 and Bcl-xL gene promoters.

Authors:  Barbara Marinari; Antonio Costanzo; Valeria Marzano; Enza Piccolella; Loretta Tuosto
Journal:  Proc Natl Acad Sci U S A       Date:  2004-04-12       Impact factor: 11.205

Review 5.  Free radicals and endothelial dysfunction: potential positive effects of TNF-α inhibitors.

Authors:  Giuseppe Murdaca; Francesca Spanò; Paola Cagnati; Francesco Puppo
Journal:  Redox Rep       Date:  2013-05-10       Impact factor: 4.412

6.  The receptor SIGIRR suppresses Th17 cell proliferation via inhibition of the interleukin-1 receptor pathway and mTOR kinase activation.

Authors:  Muhammet F Gulen; Zizhen Kang; Katarzyna Bulek; Wan Youzhong; Tae Whan Kim; Yi Chen; Cengiz Z Altuntas; Kristian Sass Bak-Jensen; Mandy J McGeachy; Jeong-Su Do; Hui Xiao; Greg M Delgoffe; Booki Min; Jonathan D Powell; Vincent K Tuohy; Daniel J Cua; Xiaoxia Li
Journal:  Immunity       Date:  2010-01-07       Impact factor: 31.745

7.  TNF-α gene polymorphisms: association with disease susceptibility and response to anti-TNF-α treatment in psoriatic arthritis.

Authors:  Giuseppe Murdaca; Rossella Gulli; Francesca Spanò; Francesca Lantieri; Martina Burlando; Aurora Parodi; Paola Mandich; Francesco Puppo
Journal:  J Invest Dermatol       Date:  2014-03-04       Impact factor: 8.551

8.  IRAK4 kinase activity is required for Th17 differentiation and Th17-mediated disease.

Authors:  Kirk A Staschke; Sucai Dong; Joy Saha; Jingyong Zhao; Nathan A Brooks; Deena L Hepburn; Jinqi Xia; Muhammet F Gulen; Zizhen Kang; Cengiz Z Altuntas; Vincent K Tuohy; Raymond Gilmour; Xiaoxia Li; Songqing Na
Journal:  J Immunol       Date:  2009-07-01       Impact factor: 5.422

9.  Fed-batch culture optimization of a growth-associated hybridoma cell line in chemically defined protein-free media.

Authors:  Xianghui Gong; Dongxiao Li; Xuesen Li; Qiangyi Fang; Xiangzong Han; Yuyin Wu; Shengli Yang; Bing Q Shen
Journal:  Cytotechnology       Date:  2006-12-02       Impact factor: 2.058

10.  Increased interleukin-17 production via a phosphoinositide 3-kinase/Akt and nuclear factor kappaB-dependent pathway in patients with rheumatoid arthritis.

Authors:  Kyoung-Woon Kim; Mi-La Cho; Mi-Kyung Park; Chong-Hyeon Yoon; Sung-Hwan Park; Sang-Heon Lee; Ho-Youn Kim
Journal:  Arthritis Res Ther       Date:  2004-11-29       Impact factor: 5.156

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