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Related Experiment Videos

Expression and function of surface antigens on scleroderma fibroblasts.

D Abraham1, S Lupoli, A McWhirter

  • 1Cell Enzymology Unit, Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, England.

Arthritis and Rheumatism
|September 1, 1991
PubMed
Summary

Systemic sclerosis (SSc) dermal fibroblasts bind more T lymphocytes due to increased intercellular adhesion molecule type 1 (ICAM-1) expression. This heightened binding, crucial in SSc pathogenesis, is mediated by ICAM-1 and lymphocyte function-associated antigen type 3 (LFA-3) interactions.

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Area of Science:

  • Immunology
  • Dermatology
  • Cell Biology

Background:

  • Systemic sclerosis (SSc) is a complex autoimmune disease characterized by fibrosis.
  • T lymphocyte interactions with dermal fibroblasts are implicated in SSc pathogenesis.
  • The molecular mechanisms underlying fibroblast-T cell adhesion in SSc require further elucidation.

Purpose of the Study:

  • To investigate the differences in T lymphocyte binding to dermal fibroblasts from SSc patients and healthy individuals.
  • To identify the specific cell adhesion molecules involved in this interaction.

Main Methods:

  • Co-culture of T lymphocytes with dermal fibroblasts from SSc patients and normal controls.
  • Use of monoclonal antibodies (MAb) targeting various cell adhesion molecules (MHC, CD4, CD8, LFA-3, CD2, ICAM-1, LFA-1).

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  • Flow cytometry to quantify cell adhesion and protein expression.

    • Main Results:

    • SSc fibroblasts exhibited significantly greater binding of T lymphocytes compared to normal fibroblasts.
    • Monoclonal antibodies against lymphocyte function-associated antigen type 3 (LFA-3) and CD2 strongly inhibited binding.
    • Monoclonal antibodies against intercellular adhesion molecule type 1 (ICAM-1) and LFA-1 (leukocyte function-associated antigen 1) inhibited binding more effectively with SSc fibroblasts and abolished cytokine-induced binding.
    • SSc fibroblasts showed higher expression levels of ICAM-1 compared to normal fibroblasts.

    Conclusions:

    • Cultured SSc dermal fibroblasts demonstrate elevated binding to T lymphocytes.
    • This increased adhesion is primarily mediated by ICAM-1 and LFA-3/CD2 pathways.
    • Elevated ICAM-1 expression on SSc fibroblasts likely contributes to enhanced T cell interactions, potentially driving SSc pathology.