Cellular interactions between synovial T-cell clones from a patient with rheumatoid arthritis

J M Van Laar, A M Miltenburg, P De Kuiper, M R Daha, R R De Vries, F C Breedveld

    Research output: Contribution to journalArticleAcademicpeer-review

    Abstract

    The aim of this study was to investigate T-T cell interactions that may be involved in the pathogenesis of chronic synovitis. Two CD4+ T-cell clones, termed N16 and N18, sharing similar cytokine profiles were isolated from the synovial tissue of a patient with rheumatoid arthritis. Activated N16 cells induced proliferation of N18 cells in the absence of accessory cells, while the proliferative response of N18 cells to activated N18 cells depended on the presence of accessory cells. Whereas the response of N18 to activated N18 cells could be blocked by MoAbs against HLA class I and LFA-1 molecules, the response of N18 to activated N16 cells was only weakly affected, suggesting that the surface molecules involved in this interaction differed. Indeed, using MoAbs against CD3, CD4 and to a lesser extent CD2, proliferation of N18 to activated N16 cells was abrogated. These data provide a model for T-T cell interactions involved in the development of chronic synovitis.

    Original languageEnglish
    Pages (from-to)651-5
    Number of pages5
    JournalScandinavian Journal of Immunology
    Volume37
    Issue number6
    Publication statusPublished - Jun 1993

    Keywords

    • Antibodies
    • Antibodies, Monoclonal
    • Antigen-Presenting Cells
    • Antigens, CD2
    • Antigens, CD3
    • Antigens, CD4
    • Antigens, CD8
    • Antigens, Differentiation, T-Lymphocyte
    • Arthritis, Rheumatoid
    • Binding, Competitive
    • Cell Communication
    • Clone Cells
    • Epitopes
    • HLA Antigens
    • Humans
    • Lymphocyte Activation
    • Receptors, Immunologic
    • Synovial Fluid
    • T-Lymphocytes
    • Journal Article
    • Research Support, Non-U.S. Gov't

    Fingerprint

    Dive into the research topics of 'Cellular interactions between synovial T-cell clones from a patient with rheumatoid arthritis'. Together they form a unique fingerprint.

    Cite this