ArticleArthritis and rheumatism2009
Unmasking of a protective tumor necrosis factor receptor I-mediated signal in the collagen-induced arthritis model.
Article in Arthritis and rheumatism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 32 citations in OpenAlex.
- Analyzing the genes and pathways related to major depressive disorder via a systems biology approach.Brain and behavior · 2020Article
- Enthesitis: Much More Than Focal Insertion Point Inflammation.Current rheumatology reports · 2018Review
- Article
- Network and Pathway-Based Analyses of Genes Associated with Parkinson's Disease.Molecular neurobiology · 2017Article
- Analyzing the genes related to Alzheimer's disease via a network and pathway-based approach.Alzheimer's research & therapy · 2017Article
- Semaphorin 4D Contributes to Rheumatoid Arthritis by Inducing Inflammatory Cytokine Production: Pathogenic and Therapeutic Implications.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Exploring the pathogenetic association between schizophrenia and type 2 diabetes mellitus diseases based on pathway analysis.BMC medical genomics · 2013Article
- Tumor necrosis factor induces GSK3 kinase-mediated cross-tolerance to endotoxin in macrophages.Nature immunology · 2011Article
- The tumour necrosis factor/TNF receptor superfamily: therapeutic targets in autoimmune diseases.Clinical and experimental immunology · 2011Article
- [Biologics. Magic bullets - magic effects - magic costs? New therapeutics and their effects].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2011Article
- A crucial role for tumor necrosis factor receptor 1 in synovial lining cells and the reticuloendothelial system in mediating experimental arthritis.Arthritis research & therapy · 2010Article
- Anti-TNF biologic agents: still the therapy of choice for rheumatoid arthritis.Nature reviews. Rheumatology · 2009Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo examine the relative importance of tumor necrosis factor receptor I (TNFRI) signaling in the hematopoietic tissue compartment in the progression of collagen-induced arthritis (CIA), a model of rheumatoid arthritis (RA).
methodsDBA/1 mice were administered a lethal radiation dose and were then rescued with bone marrow derived from either DBA/1 or TNFRI(-/-) mice. CIA was then induced, and disease progression was characterized.
resultsSurprisingly, mice with CIA that received TNFRI(-/-) donor marrow developed increased disease severity as compared with control mice with CIA. This could not be attributed to an increased primary response to collagen or to the contribution of a non-DBA genetic background. In mice that received TNFRI(-/-) bone marrow, histologic markers of advanced disease were evident shortly after initiation of the immune response to collagen and long before clinical evidence of disease. Serum TNFalpha was undetectable, whereas serum interleukin-12 p40 levels were increased, at the end point of the study in mice that received TNFRI(-/-) bone marrow.
conclusionThese data raise the intriguing possibility of the existence of an antiinflammatory, TNFRI-mediated circuit in the hematopoietic compartment. This circuit bears a resemblance to the switch in TNFalpha function that has been observed during the resolution of bacterial infections. These data suggest that TNFRI-mediated signals in the radioresistant tissues contribute to disease progression, whereas TNFRI-mediated signals in the radiosensitive tissues can contribute to protection from disease. We thus put forward the hypothesis that the degree of response to TNFalpha blockade in RA is dependent in part on the relative genetic strengths of these 2 pathways.
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