Update on D2E7: a fully human anti-tumour necrosis factor 
monoclonal antibody
Joachim Kempeni
Department of
Clinical Oncology/Immunology, Knoll AG-BASF Pharma, Knollstrasse,
D-67008 Ludwigshafen, Germany
Correspondence to: Dr Kempeni (joachim.kempeni@knoll-ag.de)
| The first 150 words of the full text of this article appear below. |
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Introduction |
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Rheumatoid arthritis (RA) is characterised by persistent joint inflammation and concomitant joint destruction, and in severe cases with extra-articular manifestations, multiple joint involvement, and a significant reduction in life expectancy. In addition, functional decline and disability inevitably accompanies joint destruction. The extent to which most standard medical approaches have a positive impact on the course of rheumatoid disease is the subject of debate.1 Intense research effort has focused on understanding cellular inflammatory mechanisms that may serve as therapeutic targets.
Tumour necrosis factor 
(TNF) is a pleiotropic cytokine
overproduced in rheumatoid joints primarily by
macrophages.2 Although the causes of RA are not fully
understood, TNF seems to play a cardinal part in a variety of events
in inflammatory synovitis and articular matrix
degradation,3 and is therefore a prime target for directed
immunotherapy in RA.4 5 Accordingly, antibodies and
soluble TNF receptors that bind TNF with high specificity neutralise
its activity and
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(2003). Scintigraphic detection of tumour necrosis factor in patients with rheumatoid arthritis. Ann Rheum Dis
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[Abstract] [Full Text]
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