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Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis

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, al...

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Autores principales: Ji, Hong, Pettit, Allison, Ohmura, Koichiro, Ortiz-Lopez, Adriana, Duchatelle, Veronique, Degott, Claude, Gravallese, Ellen, Mathis, Diane, Benoist, Christophe
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2002
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2194010/
https://www.ncbi.nlm.nih.gov/pubmed/12093872
http://dx.doi.org/10.1084/jem.20020439
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author Ji, Hong
Pettit, Allison
Ohmura, Koichiro
Ortiz-Lopez, Adriana
Duchatelle, Veronique
Degott, Claude
Gravallese, Ellen
Mathis, Diane
Benoist, Christophe
author_facet Ji, Hong
Pettit, Allison
Ohmura, Koichiro
Ortiz-Lopez, Adriana
Duchatelle, Veronique
Degott, Claude
Gravallese, Ellen
Mathis, Diane
Benoist, Christophe
author_sort Ji, Hong
collection PubMed
description 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)–α was also required, although seemingly less critically than IL-1, because a proportion of TNF-α–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 TNFα for bone destruction. The variability in the requirement for TNF-α, reminiscent of that observed in treated rheumatoid arthritis patients, did not appear genetically programmed but related instead to subtle environmental changes.
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spelling pubmed-21940102008-04-11 Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis Ji, Hong Pettit, Allison Ohmura, Koichiro Ortiz-Lopez, Adriana Duchatelle, Veronique Degott, Claude Gravallese, Ellen Mathis, Diane Benoist, Christophe J Exp Med Article 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)–α was also required, although seemingly less critically than IL-1, because a proportion of TNF-α–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 TNFα for bone destruction. The variability in the requirement for TNF-α, reminiscent of that observed in treated rheumatoid arthritis patients, did not appear genetically programmed but related instead to subtle environmental changes. The Rockefeller University Press 2002-07-01 /pmc/articles/PMC2194010/ /pubmed/12093872 http://dx.doi.org/10.1084/jem.20020439 Text en Copyright © 2002, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Ji, Hong
Pettit, Allison
Ohmura, Koichiro
Ortiz-Lopez, Adriana
Duchatelle, Veronique
Degott, Claude
Gravallese, Ellen
Mathis, Diane
Benoist, Christophe
Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis
title Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis
title_full Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis
title_fullStr Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis
title_full_unstemmed Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis
title_short Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis
title_sort critical roles for interleukin 1 and tumor necrosis factor α in antibody-induced arthritis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2194010/
https://www.ncbi.nlm.nih.gov/pubmed/12093872
http://dx.doi.org/10.1084/jem.20020439
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