The DOI matches its Crossref record; 125 of the 125 references it cites were found in a registry or an index.
Anti-TNFα Therapy of Rheumatoid Arthritis: What Have We Learned?
Abstract
Rheumatoid arthritis (RA), a systemic disease, is characterized by a chronic inflammatory reaction in the synovium of joints and is associated with degeneration of cartilage and erosion of juxta-articular bone. Many pro-inflammatory cytokines including TNFα, chemokines, and growth factors are expressed in diseased joints. The rationale that TNFα played a central role in regulating these molecules, and their pathophysiological potential, was initially provided by the demonstration that anti-TNFα antibodies added to in vitro cultures of a representative population of cells derived from diseased joints inhibited the spontaneous production of IL-1 and other pro-inflammatory cytokines. Systemic administration of anti-TNFα antibody or sTNFR fusion protein to mouse models of RA was shown to be anti-inflammatory and joint protective. Clinical investigations in which the activcity of TNFα in RA patients was blocked with intravenously administered infliximab, a chimeric anti-TNFα monoclonal antibody (mAB), has provided evidence that TNF regulates IL-6, IL-8, MCP-1, and VEGF production, recruitment of immune and inflammatory cells into joints, angiogenesis, and reduction of blood levels of matrix metalloproteinases-1 and -3. Randomized, placebo-controlled, multi-center clinical trials of human TNFα inhibitors have demonstrated their consistent and remarkable efficacy in controlling signs and symptoms, with a favorable safety profile, in approximately two thirds of patients for up to 2 years, and their ability to retard joint damage. Infliximab (a mAB), and etanercept (a sTNF-R-Fc fusion protein) have been approved by regulatory authorities in the United States and Europe for treating RA, and they represent a significant new addition to available therapeutic options.
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Cites
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Self-citationAnti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia
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Cited by
NF-κB signaling in inflammation
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Signalling pathways of the TNF superfamily: a double-edged sword
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Kaminska, B. (2005) · Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics · doi:10.1016/j.bbapap.2005.08.017 · Cited by 1,285
IL-6 in autoimmune disease and chronic inflammatory proliferative disease
Ishihara, K., & Hirano, T. (2002) · Cytokine & Growth Factor Reviews · doi:10.1016/s1359-6101(02)00027-8 · Cited by 807
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Self-citation
Metadata
- Authors
- Feldmann, M., & Maini, R. N.
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 2001-04
- Volume
- 19
- Issue
- 1
- Pages
- 163-196
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- OpenAlex
- W2134714663
- Cited by
- 1,257
- References
- 125
- FWCI
- 9.29
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
