Critical roles for interleukin 1 and tumor necrosis factor alpha in antibody-induced arthritis

Ji, H, Pettit, A, Ohmura, K, Ortiz-Lopez, A, Duchatelle, V, Degott, C, Gravallese, E, Mathis, D and Benoist, C (2002) Critical roles for interleukin 1 and tumor necrosis factor alpha in antibody-induced arthritis. Journal of Experimental Medicine, 196 1: 77-85. doi:10.1084/jem.20020439

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Author Ji, H
Pettit, A
Ohmura, K
Ortiz-Lopez, A
Duchatelle, V
Degott, C
Gravallese, E
Mathis, D
Benoist, C
Title Critical roles for interleukin 1 and tumor necrosis factor alpha in antibody-induced arthritis
Journal name Journal of Experimental Medicine   Check publisher's open access policy
ISSN 0022-1007
Publication date 2002-01-01
Sub-type Article (original research)
DOI 10.1084/jem.20020439
Open Access Status File (Publisher version)
Volume 196
Issue 1
Start page 77
End page 85
Total pages 9
Place of publication New York
Publisher Rockefeller Univ Press
Language eng
Abstract in spontaneous inflammatory arthritis of K/BxN T cell receptor transgenic mice, the effector phase of the disease is provoked by binding of immunoglobulins (Igs) to joint surfaces. Inflammatory cytokines are known to be involved in human inflammatory arthritis, in particular rheumatoid arthritis, although, overall, the pathogenetic mechanisms of the human affliction remain unclear. To explore the analogy between the K/BxN model and human patients, we assessed the role and relative importance of inflammatory cytokines in K/BxN joint inflammation by transferring arthritogenic serum into a panel of genetically deficient recipients. Interleukin (IL)-1 proved absolutely necessary. Tumor necrosis factor (TNF)-alpha was also required, although seemingly less critically than IL-1, because a proportion of TNF-alpha-deficient mice developed robust disease. There was no evidence for an important role for IL-6. Bone destruction and reconstruction were also examined. We found that all mice with strong inflammation exhibited the bone erosion and reconstruction phenomena typical of K/BxN arthritis, with no evidence of any particular requirement for TNFalpha for bone destruction. The variability in the requirement for TNF-alpha, reminiscent of that observed in treated rheumatoid arthritis patients, did not appear genetically programmed but related instead to subtle environmental changes.
Keyword Immunology
Medicine, Research & Experimental
transgenic
cytokine
knockout
inflammatory
TNF
Collagen-induced Arthritis
Ameliorates Joint Disease
Antigen-induced Arthritis
Receptor-deficient Mice
Rheumatoid-arthritis
T-cell
Factor-alpha
Tnf-alpha
Interleukin-6-deficient Mice
Inflammatory Response
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: Institute for Molecular Bioscience - Publications
 
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Created: Wed, 17 Oct 2007, 21:11:48 EST