Mast Cells: A Cellular Link Between Autoantibodies and Inflammatory Arthritis

By David M. Lee, D. Friend, M. Gurish, C. Benoist, D. Mathis, M. Brenner. Science, 2002

853 citations recorded by the source corpus.

Subfields: Immunology, Physiology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/16bd2bbb969dc985c780a800f87dfed7b8684619

How researchers see this paper

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

In Immunology

1. S. Galli
2. M. Tsai
3. John D Lambris
4. M. Markiewski
5. Peter Libby
6. C. Nathan
7. Georg Schett
8. Gary S. Firestein

In Physiology

1. S. Galli
2. M. Tsai
3. Peter Libby
4. C. Nathan
5. G. Palmer
6. B. Kahn
7. C. Gabay
8. W. Arend

In Rheumatology

1. I. McInnes
2. Gary S. Firestein
3. Georg Schett
4. Peter Libby
5. S. Galli
6. S. Gaffen

Citations in the corpus

• Immunomodulatory mast cells: negative, as well as positive, regulators of immunity (2008, background): “Mast cells can also make a substantial contribution to disease pathology in models of autoantibody-induced destructive arthriti”
• Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. (2003, background): “Mast cells play a critical role in murine arthritis and bullous pemphigoid induced by passive transfer of Ab’s (43, 44).”
• Evolving concepts of rheumatoid arthritis (2003, background): “Innate immunity also participates in antibody-mediated arthritis, and mast cells are required for the disease onset of some model”
• The role of complement in inflammatory diseases from behind the scenes into the spotlight. (2007, background): “Mast cells and neutrophils that are activated by complement anaphylatoxins release mediators that cause vasodilation and extravasation of fluid.(19) Another cell population that is activated at the very beginning of the inflammatory reaction are the macrophages, which are found in large numbers in c”
• IL‐1, IL‐18, and IL‐33 families of cytokines (2008, background): “Interestingly, mast cells have been recognized as important mediators of the pathogenesis of arthritis (201, 202), suggesting a role for IL-33-mediated mast cell activation in joint inflammation.”
• Points of control in inflammation (2002, background): “The importance of mast cells as first responders (see review in this issue by Benoist and Mathis, pages 875–878 ), recently emphasized in experimental rheumatoid arthriti”
• Five years of GWAS discovery. (2012, background): “Although its function remains unclear, genetic variants near ORMDL3 are associated with various immune-related diseases, including asthma, type 1 diabetes, Crohn’s diseases, ulcerative colitis and primary biliary cirrhosis [25]–[29].”
• Deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice (2009, background): “Mast cell stabilizer ketotifen [4-(1-methyl4-piperidylidene)-4h-benzo[4,5]cyclohepta[1,2-b]thiophen-10(9H)-one fumarate] prevents mucosal mast cell hyperplasia and intestinal dysmotility in experimental Trichinella spiralis inflammation in the rat.”
• Cytokines in the pathogenesis of rheumatoid arthritis (2007, background): “Studies involving the transfer of arthritogenic serum from the K/BxN-transgenic mouse model to mast-cell-deficient ( W/Wv ) mice clearly demonstrate integration of immune-complex-, complement- and cytokine- (particularly IL-1 and TNF) mediated synovial inflammatio”