Recognition of the 60 kilodalton cysteine‐rich outer membrane protein OMP2 by CD4+ T cells from humans infected with Chlamydia trachomatis
T cell‐mediated immunity is important in the control of chlamydia infection but chlamydia‐specific T cells are also implicated in the inflammation and tissue damage which characterize chlamydia associated diseases. To investigate target antigens of the T cell‐mediated immune response to chlamydia in...
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Published in | Clinical and experimental immunology Vol. 126; no. 3; pp. 488 - 493 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Science Ltd
01.12.2001
Blackwell Oxford University Press Blackwell Science Inc |
Subjects | |
Online Access | Get full text |
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Summary: | T cell‐mediated immunity is important in the control of chlamydia infection but chlamydia‐specific T cells are also implicated in the inflammation and tissue damage which characterize chlamydia associated diseases. To investigate target antigens of the T cell‐mediated immune response to chlamydia infection, Chlamydia trachomatis‐specific CD4+ T cell clones were isolated from a patient with chlamydia‐induced reactive arthritis. T cell immunoblotting indicated that an antigen of ∼60 kilodaltons molecular mass was recognized, and recombinant 60 kilodalton cysteine‐rich outer membrane 2 (OMP2) proved to be stimulatory. By using deletion constructs and synthetic peptides an epitope presented by HLA‐DRB1*0401 was defined and proved to contain the nonamer peptide within the OMP2 sequence predicted to have the greatest binding affinity for DRB1*0401 The sequence of the epitope is conserved in all C. trachomatis strains but not in C. pneumoniae. Investigation of patients with acute urethritis and additional patients with sexually acquired reactive arthritis showed that OMP2‐reactive T cells were readily detectable in peripheral blood and synovial fluid. Thus OMP2 is a target antigen of the T cell‐mediated immune response to CT infection. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Present address: Department of Immunology, University of Glasgow, Glasgow, UK Present address: Department of Neurology, University of Birmingham, Birmingham, UK |
ISSN: | 0009-9104 1365-2249 |
DOI: | 10.1046/j.1365-2249.2001.01709.x |