J
J. S. H. Gaston
Researcher at University of Birmingham
Publications - 14
Citations - 725
J. S. H. Gaston is an academic researcher from University of Birmingham. The author has contributed to research in topics: Antigen & Synovial fluid. The author has an hindex of 11, co-authored 14 publications receiving 724 citations.
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Journal Article
In vitro responses to a 65-kilodalton mycobacterial protein by synovial T cells from inflammatory arthritis patients.
TL;DR: The results suggest that the 65-kDa molecule, which is common to a wide range of bacteria, may be an important immunogen for the T cell-mediated immune responses within the joint in different clinically defined inflammatory arthropathies.
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Recognition of a mycobacteria-specific epitope in the 65-kD heat-shock protein by synovial fluid-derived T cell clones.
TL;DR: Joint inflammation could not be attributed to bacteria-induced T cell clones cross-reacting with the self 65-kD Ag, because the epitope is in a portion of the 65- kD sequence that is not conserved between bacteria and eukaryotes.
Journal Article
Synovial T lymphocyte recognition of organisms that trigger reactive arthritis.
J. S. H. Gaston,P. F. Life,K Granfors,R Merilahti-Palo,L. C. Bailey,S Consalvey,Auli Toivanen,Paul A. Bacon +7 more
TL;DR: Results indicate that a bacteria-specific, T-cell-mediated response may play a central role in the pathogenesis of ReA, and that bacterial antigens localize in the joint.
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Isolation of Yersinia-specific T cell clones from the synovial membrane and synovial fluid of a patient with reactive arthritis.
TL;DR: This is the first report of the isolation of Yersinia-specific T cell clones fromsynovial membrane (obtained by closed-needle synovial biopsy) and a detailed analysis of these clones, together with others obtained from the SF.
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Synovial fluid antigen-presenting cells unmask peripheral blood T cell responses to bacterial antigens in inflammatory arthritis.
TL;DR: The contrasting responses of SFMC and PBMC to bacterial antigens may be accounted for at least in part by an enhanced ability of SF APC to support T cell proliferative responses.