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• W2110135215 endingPage "4038" @default.
• W2110135215 startingPage "4033" @default.
• W2110135215 abstract "Abstract There is a strong association between seronegative arthritis and HLA B27, but it is still unresolved whether the contribution of B27 to disease pathogenesis is solely as a restriction element for an arthritogenic peptide, or whether B27 itself serves as an autoantigen. This study uses transgenic rats to address the question as to whether exposure to an arthritogenic pathogen can alter tolerance to B27. Unlike their nontransgenic counterparts, B27-transgenic rats are tolerant of B27 immunization using either B27+ splenocytes or plasmid DNA and do not develop anti-B27 CTL. However, if splenocytes from such immunized animals are exposed to Chlamydia in vitro, CTL are generated that lyse B27+ targets. No killing was seen with targets transfected with control B7, B14, B40, or B44. This phenomenon was not observed with immunization by nontransgenic splenocytes, or HLA-A2 DNA alone. Using targets expressing mutated B27, we show that the epitope for autoreactive CTL recognition of B27 involves the Lys70 amino acid residue in the α1 domain of the MHC class I molecule. The generation of CTL with specificity for B27 under these conditions demonstrates that tolerance to B27 can be subverted by Chlamydia. This indicates a dynamic interrelationship between the pathogen and B27, which may have important implications for B27-related spondyloarthropathies triggered by intracellular bacteria." @default.
• W2110135215 created "2016-06-24" @default.
• W2110135215 creator A5013191829 @default.
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• W2110135215 date "2002-10-01" @default.
• W2110135215 modified "2023-10-16" @default.
• W2110135215 title "Breakdown of CTL Tolerance to Self HLA-B*2705 Induced by Exposure to <i>Chlamydia</i> <i>trachomatis</i>" @default.
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• W2110135215 doi "https://doi.org/10.4049/jimmunol.169.7.4033" @default.
• W2110135215 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12244206" @default.
• W2110135215 hasPublicationYear "2002" @default.
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