Treatment of rheumatoid arthritis by selective inhibition of T-cell activation with fusion protein CTLA4Ig.

By J. Kremer, R. Westhovens, M. Léon, E. Di Giorgio, R. Alten, S. Steinfeld, A. Russell, M. Dougados, P. Emery, I. Nuamah and 4 more. New England Journal of Medicine, 2003

1,063 citations recorded by the source corpus.

Subfields: Immunology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/8346397c9a9369ff7ac2331bf0b93260f25f884b

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In Immunology

1. Lieping Chen
2. W. Zou
3. Xue Han
4. D. Pardoll

In Rheumatology

1. S. Rose‐John

Citations in the corpus

• Co-inhibitory molecules of the B7–CD28 family in the control of T-cell immunity (2004, background): “Decoy CTLA4 receptor (CTLA4– immunoglobulin fusion protein) has been extensively tested in experimental models and in clinical trials for its immunosuppressive function”
• Effects of Abatacept in Patients with Methotrexate-Resistant Active Rheumatoid Arthritis (2006, methodology): “The phase III AIM study confirmed and extended the findings of a phase IIb study in a similar patient population (8, 9) by demonstrating that abatacept, with background methotrexate, is effective in reducing the signs and symptoms of rheumatoid arthritis and improving physical function and health-re”
• Rational Development of LEA29Y (belatacept), a High‐Affinity Variant of CTLA4‐Ig with Potent Immunosuppressive Properties (2005, background): “More recently, the efficacy of this molecule in the treatment of human rheumatoid arthritis has been demonstrated (11).”
• Ido expression by dendritic cells: tolerance and tryptophan catabolism (2004, neutral): “However, recent encouraging results from phase II clinical trials of recombinant CTLA4–immunoglobulin fusion protein in autoimmune rheumatoid arthriti”
• Synovial fibroblasts: key players in rheumatoid arthritis. (2006, background): “Therapeutic strategies beyond cytokine targets include the recent use of CTLA4Ig, a fusion protein that interferes with the binding of CD80/CD86 to the MHC-independent T-cell surface molecule CD28 preventing its activation [90], as well as rituximab (monoclonal antibodies against CD20) that was orig”