Evolving concepts of rheumatoid arthritis

By Gary S. Firestein. Nature, 2003

3,745 citations recorded by the source corpus.

Subfields: Radiology, Nuclear Medicine and Imaging, Rheumatology

View Paper: https://www.semanticscholar.org/paper/edfa6d908ad6c0ef6b7e8ac7616a1f4b6ab86b6b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Radiology, Nuclear Medicine and Imaging

1. Gordon D. Brown
2. I. McInnes
3. Georg Schett
4. B. Bartok
5. J. Smolen
6. Gary S. Firestein

In Rheumatology

1. I. McInnes
2. Gary S. Firestein
3. Georg Schett
4. Daniel Aletaha
5. Gordon D. Brown
6. B. Bartok
7. J. Smolen
8. David Altshuler

Citations in the corpus

• 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative (2010, positive): “the presence of autoantibodies, such as rheumatoid factor (RF) and anti–citrullinated protein antibody (ACPA) (tested as anti–cyclic citrullinated peptide [antiCCP]), which can precede the clinical manifestation of RA by many years (6–9), RA is considered an autoimmune disease (10,11).”
• Autoimmune disorders and risk of non-Hodgkin lymphoma subtypes: a pooled analysis within the InterLymph Consortium. (2008, neutral): “Median (range) 60 (17-89) 58 (16-96) Education/SES†”
• Dectin-1: a signalling non-TLR pattern-recognition receptor (2006, background): “Rheumatoid arthritis is a chronic inflammatory autoimmune disease of the joints that is characterized by changes in the synovial membranes and is thought to be mediated by self-reactive T cell”
• Cytokines in the pathogenesis of rheumatoid arthritis (2007, background): “It affects 1% of the population and is associated with significant morbidity and increased mortalit”
• Immunopathogenesis of rheumatoid arthritis (2017, neutral): “…predominantly post-translationally modified proteins, dysregulated cytokine networks, osteoclast and chondrocyte activation, and imprinting of resident stromal cells that in turn develop semi-autonomous features that support disease progression (Arend and Firestein, 2012; Firestein, 2003).”
• Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis (2010, background): “Other subsets undoubtedly exist and await the development of therapies that target other pathways or cell lineages, such as macrophages or dendritic cells (2).”
• Replication of putative candidate-gene associations with rheumatoid arthritis in >4,000 samples from North America and Sweden: association of susceptibility with PTPN22, CTLA4, and PADI4. (2005, background): “both a genetic and an environmental basis (Firestein 2003).”
• 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. (2010, neutral): “the presence of autoantibodies, such as rheumatoid factor (RF) and anti–citrullinated protein antibody (ACPA) (tested as anti–cyclic citrullinated peptide [antiCCP]), which can precede the clinical manifestation of RA by many years (6–9), RA is considered an autoimmune disease (10,11).”