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Ann Rheum Dis. 1999 Nov;58 Suppl 1:I40-8.

Role of tumour necrosis factor alpha in experimental arthritis: separate activity of interleukin 1beta in chronicity and cartilage destruction.

van den Berg WB, Joosten LA, Kollias G, van De Loo FA.

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Department of Rheumatology, University Hospital Nijmegen, the Netherlands.

Abstract

Chronic arthritis is characterised by persistent joint inflammation and concomitant joint destruction. Using murine arthritis models and neutralising antibodies as well as cytokine specific knockout conditions, it was found that tumour necrosis factor alpha (TNFalpha) is important in early joint swelling. Membrane bound TNFalpha is sufficient to drive this aspect of inflammation as well as the acute cellular infiltrate in the synovial tissue. Interleukin 1 (IL1) is not necessarily a dominant cytokine in early joint swelling, but has a pivotal role in sustained cellular infiltration and erosive cartilage damage. TNFalpha independent IL1 production is a prominent feature in murine arthritis models. These observations provide evidence for potential uncoupling of joint inflammation and erosive changes, implying that both cytokines need to be targeted to achieve optimal treatment.

PMID:: 10577972; [PubMed - indexed for MEDLINE]
PMCID:: PMC1766568

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Review TNF alpha and IL-1 beta are separate targets in chronic arthritis. [Clin Exp Rheumatol. 1999]
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Cited by 12 PubMed Central articles

A crucial role for tumor necrosis factor receptor 1 in synovial lining cells and the reticuloendothelial system in mediating experimental arthritis. [Arthritis Res Ther. 2010]
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