Prevention of Collagen-Induced Arthritis with an Antibody to gp39, the Ligand for CD40

Durie, Fiona H.; Fava, Roy A.; Foy, Teresa M.; Aruffo, Alejandro; Ledbetter, Jeffrey A.; Noelle, Randolph J.

doi:10.1126/science.7689748

Cited by 455 publications

(282 citation statements)

References 18 publications

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“…Alternatively, it is likely that future studies will also evaluate cotreatments with specific biologic agents to interfere with T cell helper signals, such as blocking antibodies to CD40-CD40 ligand (44,45) or the use of CTLA4-Ig (46). As an alternative approach, it may be desirable to utilize agents that block the recently discovered BLyS/BAFF/ zTNF4 system (for review, see ref.…”

Section: Mechanisms Of Autoimmunity and Rituximabmentioning

confidence: 99%

Rituximab therapy and autoimmune disorders: Prospects for anti–B cell therapy

Silverman¹,

Weisman²

2003

Arthritis & Rheumatism

344

204

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Section: Mechanisms Of Autoimmunity and Rituximabmentioning

confidence: 99%

Rituximab therapy and autoimmune disorders: Prospects for anti–B cell therapy

Silverman¹,

Weisman²

2003

Arthritis & Rheumatism

344

204

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“…Foy et al, 1995 , and CD40-CD40L interactions are involved in experimental autoimmune disease such as col-Ž . lagen-induced arthritis Durie et al, 1993 and lupus Ž . nephritis Mohan et al, 1995 .…”

Section: Accessory Molecules: Cd40-cd40lmentioning

confidence: 99%

Expression of accessory molecules and cytokines in acute EAE in marmoset monkeys (Callithrix jacchus)

Laman

Meurs²,

Schellekens³

et al. 1998

Journal of Neuroimmunology

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Ž .Accessory molecules and cytokines are involved in the immunopathogenesis of multiple sclerosis MS and experimental autoimmune Ž . encephalomyelitis EAE in rodent models, and are potential targets for immunotherapy. Evaluation of such experimental therapies requires appropriate animal models. Therefore, we analysed the expression of selected accessory molecules and cytokines in the brain of Ž . marmoset monkeys Callithrix jacchus with acute EAE, a newly described non-human primate model for MS. All animals experienced active disease clinically and histopathologically with strong resemblance to MS. Perivascular infiltrates of mononuclear cells showed abundant expression of CD40. CD40 was expressed on macrophages, indicating that T cell priming and macrophage effector functions Ž . Ž . may result from local CD40-CD40L interactions. CD40 ligand CD40L and B7-2 CD86 were also expressed, but to a lower extent, Ž . while B7-1 CD80 expression was limited. Both pro-inflammatory and anti-inflammatory cytokines were produced within individual Ž . lesions during active disease IFN-a, IFN-g , TNF-a, IL-1a , IL-1b, IL-2, IL-4, IL-10 and IL-12 . This suggests that relative levels rather than sequential expression of Th1-and Th2-type cytokines determine disease activity. These findings demonstrate the value of EAE in marmoset monkeys as a model to assess the role of accessory molecules and cytokines in multiple sclerosis, and to evaluate targeted intervention. q

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“…The ligation of CD40 augments the production of IL-12 in synovial cells and synovial fluid macrophages from RA patients (10,11) and enhances the expression of CD54, CD106, IL-6 (12), stromal cell-derived factor 1 (13), and vascular endothelial cell growth factor (14). In vivo, treatment with a monoclonal antibody (mAb) against CD154 prevents the development of type II collagen-induced arthritis in mice (15). These data indicate the relevance of the CD40-CD154 interaction in the immunopathogenesis of RA.…”

mentioning

confidence: 99%

Amplification of the synovial inflammatory response through activation of mitogen‐activated protein kinases and nuclear factor κB using ligation of CD40 on CD14+ synovial cells from patients with rheumatoid arthritis

Harigai¹,

Hara²,

Kawamoto³

et al. 2004

Arthritis & Rheumatism

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Objective. To determine the signal transduction pathways in CD14؉ synovial cells from patients with rheumatoid arthritis (RA) after CD40 ligation, and to examine their role in amplifying synovial inflammation in affected joints.Methods. Expression of messenger RNA was analyzed using quantitative reverse transcriptionpolymerase chain reaction. Cytokines and chemokines were measured using enzyme-linked immunosorbent assay. Activation of kinases was detected using Western blotting. Nuclear translocation of NF-B was examined using immunohistochemistry. CD14؉ synovial cells were enriched using magnetic cell sorting. Fibroblastlike synoviocytes (FLS) were obtained by passaging primary synovial cell culture.Results. Stimulation of CD14؉ synovial cells from RA patients by recombinant soluble CD154 (rsCD154) significantly induced expression of tumor necrosis factor ␣ (TNF␣),

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Prevention of Collagen-Induced Arthritis with an Antibody to gp39, the Ligand for CD40

Cited by 455 publications

References 18 publications

Rituximab therapy and autoimmune disorders: Prospects for anti–B cell therapy

Rituximab therapy and autoimmune disorders: Prospects for anti–B cell therapy

Expression of accessory molecules and cytokines in acute EAE in marmoset monkeys (Callithrix jacchus)

Amplification of the synovial inflammatory response through activation of mitogen‐activated protein kinases and nuclear factor κB using ligation of CD40 on CD14+ synovial cells from patients with rheumatoid arthritis

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