Cationic Yersinia antigen-induced chronic allergic arthritis in rats. A model for reactive arthritis in humans.

@article{Mertz1991CationicYA,
  title={Cationic Yersinia antigen-induced chronic allergic arthritis in rats. A model for reactive arthritis in humans.},
  author={Andreas K. H. Mertz and Steven Batsford and Enrico Curschellas and Manfred Kist and K B Gondolf},
  journal={The Journal of clinical investigation},
  year={1991},
  volume={88 2},
  pages={
          632-42
        }
}
Cationic antigens are known to have considerable arthritogenic potential in experimental systems. During a systematic search for suitable, naturally occurring candidates an intracellular protein was isolated from the ribosomal pellet of Yersinia enterocolitica 0:3, a bacterial strain associated with reactive arthritis in humans. The protein is highly cationic, contains two 19-kD polypeptide chains linked by a disulfide bond, and reveals a strong tendency for spontaneous aggregation. It is… 
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Identification of the Yersinia enterocolitica urease beta subunit as a target antigen for human synovial T lymphocytes in reactive arthritis
TLDR
Analysis of the T-cell response to a 19-kDa antigen of Yersinia enterocolitica O:9 showed that it contains several T- cell epitopes, one of which cross-reacts with other enterobacteria not able to induce ReA, indicating that the arthritogenicity of the19-k da antigen is not a property of the 19-KDa protein alone but is dependent on its expression in bacteria able to induced ReA.
Characterization of the synovial T cell response to various recombinant Yersinia antigens in Yersinia enterocolitica-triggered reactive arthritis. Heat-shock protein 60 drives a major immune response.
TLDR
In Y enterocolitica-triggered ReA, at least 4 immunodominant T cell antigens exist, which might be used in lymphocyte proliferation assays to identify patients with Yersinia ReA.
Enterobacterial antigens with tropism for joint structures and HLA-B27-restricted cytotoxic T-cells in reactive arthritis.
  • E. Hermann
  • Medicine, Biology
    Scandinavian journal of rheumatology. Supplement
  • 1995
TLDR
This group has focussed attention on the T cellular immune events at the site of synovitic inflammation, and favors the concept of deposition of bacterial components in the synovial compartment of ReA patients.
Aetiological agents and immune mechanisms in enterogenic reactive arthritis.
Conserved Bacterial Proteins: Implications for the Pathogenesis of Reactive Arthritis
Role of T-cells in the development of arthritis.
  • J. Gaston
  • Medicine, Biology
    Clinical science
  • 1998
TLDR
Animal studies indicate that autoimmune/inflammatory diseases can be produced by imbalances within T-cell populations, and that certain T-cells also have the capacity to regulate inflammatory responses and may play a part in the pathogenesis of arthritis.
Role of T-cells in the development of arthritis
TLDR
Animal studies indicate that autoimmune/inflammatory diseases can be produced by imbalances within T-cell populations, and that certain T-cells also have the capacity to regulate inflammatory responses and may play a part in the pathogenesis of arthritis.
The Evolutionarily Conserved Ribosomal Protein L23 and the Cationic Urease β-Subunit of Yersinia enterocolitica O:3 Belong to the Immunodominant Antigens in Yersinia-Triggered Reactive Arthritis: Implications for Autoimmunity
TLDR
Sharing of conserved immunodominant proteins between different disease triggering microorganisms could provide an explanation of the shared clinical picture in Reactive arthritis.
Arthritis and Foodborne Bacteria.
TLDR
A few studies have demonstrated that T-cells from the joints of arthritic patients respond to both bacterial and human heat shock proteins indicating that autoimmunity may be involved in causation of arthritis.
Experimental Yersinia enterocolitica infection in rodents: A model for human yersiniosis
TLDR
The experimental rat model turned out to be a suitable model for studying Yersinia‐induced aseptic arthritis and expression of YadA, the collagen‐binding factor, was not necessary for arthritis induction, and a close association between both susceptibility to arthritis induction and Yersinian infection could be demonstrated in various rat strains.
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