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Related Concept Videos

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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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Related Experiment Video

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Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis
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Mast cells in rheumatic disease.

Jolien Suurmond1, Daniël van der Velden2, Johan Kuiper3

  • 1Department of Rheumatology, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC Leiden, The Netherlands.

European Journal of Pharmacology
|May 7, 2015
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Summary

Rheumatoid arthritis involves complex autoimmune pathways causing joint inflammation. Mast cell activation in rheumatoid arthritis may contribute to disease pathogenesis and tissue destruction.

Keywords:
AutoantibodiesChronic inflammationCromoglicate lisetil (PubChem CID: 196639)Cromolyn sodium salt (PubChem CID: 16219066)Histamine (PubChem CID: 774)Interleukin-8 (PubChem CID: 44357137)Leukotriene B4 (PubChem CID: 5280492)Mast cellsRheumatoid arthritisSalbutamol (PubChem CID: 2083)Toll like receptors

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Area of Science:

  • Immunology
  • Rheumatology
  • Pathogenesis of Autoimmune Diseases

Background:

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial tissue inflammation and destruction.
  • Immune pathways involving autoantibodies, Toll-Like Receptor ligands, and cytokines contribute to RA's pro-inflammatory environment.
  • Mast cells are immune cells that can be activated by these pathways, releasing inflammatory mediators.

Purpose of the Study:

  • To explore the potential role of mast cell activation in the pathogenesis of rheumatoid arthritis.
  • To understand how mast cell mediators contribute to inflammation and tissue destruction in RA.

Main Methods:

  • Review of molecular pathways involved in RA pathogenesis.
  • Analysis of the role of mast cells and their mediators in inflammatory processes.
  • Examination of evidence linking mast cell activation to synovial tissue changes in RA patients.

Main Results:

  • Multiple immune pathways converge to activate mast cells in RA.
  • Mast cell activation leads to the release of cytokines, chemokines, and proteases that recruit leukocytes.
  • Mast cell mediators can promote tissue remodeling and fibroblast activation, potentially contributing to joint damage.

Conclusions:

  • Mast cell activation is implicated in rheumatoid arthritis pathogenesis.
  • Increased mast cells and mediators in RA synovial tissue suggest a significant role in disease progression.
  • Further research is needed to elucidate the precise functional role of mast cells in arthritis, particularly in mouse models.