Association between reactive arthritis and antecedent infection with <i>shigella flexneri</i> carrying a 2‐md plasmid and encoding an hla–b27 mimetic epitope

Stieglitz, Heather; Lipsky, PE

doi:10.1002/art.1780361010

Cited by 32 publications

(16 citation statements)

References 6 publications

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“…Shigella DNA has not been convincingly demonstrated in the joints of ReA patients, making it more likely that only pieces of bacteria are transported to the joints. It has been reported that only Shigella strains containing the pHS-2 plasmid are arthritogenic (180,191). pHS-2 influences invasiveness and intracellular and intercellular movement and hence is important for the mechanism of infection.…”

Section: Bacterium-host Interactionmentioning

confidence: 99%

HLA-B27-Associated Reactive Arthritis: Pathogenetic and Clinical Considerations

2004

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Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable, nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. The mechanisms that lead to the development of ReA are complex and basically involve an interaction between an arthritogenic agent and a predisposed host. The way in which a host accommodates to invasive facultative intracellular bacteria is the key to the development of ReA. The details of the molecular pathways that explain the articular and extra-articular manifestations of the disease are still under investigation. Several studies have been done to gain a better understanding of the pathogenesis of ReA; these constitute the basis for a more rational therapeutic approach to this disease

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Section: Bacterium-host Interactionmentioning

confidence: 99%

HLA-B27-Associated Reactive Arthritis: Pathogenetic and Clinical Considerations

2004

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“…We know that there are more than 100 subsets of HLA B27 9 and we know the amino acid sequence for each of the B27 subsets. We know that there are specific infections like Salmonella 10 and Shigella 11 that trigger reactive arthritis. There is even sex to intrigue the reader of this mystery novel since we know that non-gonococcal urethritis is a clear trigger for reactive arthritis 12 .…”

Section: Introductionmentioning

confidence: 99%

Does the Microbiome Cause B27-related Acute Anterior Uveitis?

Rosenbaum

Lin

Asquith

2016

Ocular Immunology and Inflammation

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The microbiome is strongly implicated in a broad spectrum of immune-mediated diseases. Data support the concept that HLA molecules shape the microbiome. We provide hypotheses to reconcile how HLA B27 might affect the microbiome and in turn predispose to acute anterior uveitis. These theories include bacterial translocation, antigenic mimicry, and dysbiosis leading to alterations in regulatory and effector T cell subsets.

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“…84-86 It was found that Shigella flexneri strains that are isolated from ReA patients carry a plasmid (pHS-2) 86. DNA sequence analyses of this plasmid revealed that it contains an open reading frame (ORF) encoding a 22 amino acid peptide with sequence homology to B27, again involving the sequence QTDR—that is, GTVCAQTDRHSLSCIAMQ.…”

Section: Resultsmentioning

confidence: 99%

HLA-B27 associated spondyloarthropathy, an autoimmune disease based on crossreactivity between bacteria and HLA-B27?

Ringrose

1999

Annals of the Rheumatic Diseases

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Most autoimmune diseases are associated with certain HLA types. Therefore, spondyloarthropathies (SpA) strongly associated with HLA-B27, are also often classified as autoimmune diseases. This study questions whether SpA indeed fulfils the criteria of an autoimmune disease. The Medline database was searched for all reports between 1966 and April 1998 on the presence of autoimmune reactivity in SpA patients. This search yielded 45 articles on this subject. Only eight articles study T cell reactivity. Twelve reports were found on the assessment of antibodies crossreacting between bacteria and HLA-B27. In the 45 studies demonstrating autoimmune reactions in SpA patients proper controls matched for HLA-B27, sex and age were nearly always lacking. Therefore, it is concluded that the frequency of increased autoreactivity in sera from patients and controls is not significantly diVerent, and that this lack of autoreactivity does not justify classification of SpA as an autoimmune disease. As crossreactive antibodies against bacteria and HLA-B27 were equally present in sera from patients and controls, the pathogenetic significance of molecular mimicry between various bacteria and HLA-B27 is questionable. Furthermore, the regions of the B27 molecule that are supposed to be crossreactive with bacteria, diVer in one or more amino acids among the distinct B27 subtypes. Although these diVerences strongly influence the binding of antibodies to the B27 molecule, there was no relation between the degree of crossreactivity of certain subtypes and the association of these subtypes with SpA. In conclusion, there is no evident proof that SpA is an autoimmune disease attributable to crossreactivity between bacteria and HLA-B27. (Ann Rheum Dis 1999;58:598-610)

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Association between reactive arthritis and antecedent infection with shigella flexneri carrying a 2‐md plasmid and encoding an hla–b27 mimetic epitope

Cited by 32 publications

References 6 publications

HLA-B27-Associated Reactive Arthritis: Pathogenetic and Clinical Considerations

HLA-B27-Associated Reactive Arthritis: Pathogenetic and Clinical Considerations

Does the Microbiome Cause B27-related Acute Anterior Uveitis?

HLA-B27 associated spondyloarthropathy, an autoimmune disease based on crossreactivity between bacteria and HLA-B27?

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