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New perspective on Behçet's disease

T Sakane1

  • 1Department of Immunology, St. Marianna University, School of Medicine, Kanagawa, Japan.

International Reviews of Immunology
|January 1, 1997
PubMed
Summary
This summary is machine-generated.

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Behçet's syndrome, particularly along the Silk Route, involves neutrophil hyperfunction linked to HLA-B51 and T cell responses to heat shock proteins (HSP). This suggests a molecular mimicry mechanism in its autoimmune nature.

Area of Science:

  • Immunology
  • Rheumatology
  • Genetics

Background:

  • Behçet's disease exhibits distinct characteristics along the Silk Route, including genetic factors, neutrophil involvement, and disease severity.
  • The term "Behçet's syndrome" is preferred over "Behçet's disease" to better encompass its complex presentation.

Purpose of the Study:

  • To investigate the role of HLA-B51 in neutrophil hyperfunction in Behçet's disease.
  • To explore T cell responses to heat shock proteins (HSP) and their potential role in the autoimmune pathogenesis of Behçet's disease.
  • To elucidate the molecular mimicry mechanisms potentially underlying Behçet's disease.

Main Methods:

  • Correlation analysis between neutrophil hyperfunction and HLA-B51 phenotype in humans and HLA-B transgenic mice.
  • T cell proliferation assays using a specific peptide from human heat shock protein (HSP)-60.

Related Experiment Videos

  • Analysis of T cell receptor (TCR) V beta subfamily usage via monoclonal antibodies, PCR, and single-strand conformation polymorphism.

    • Main Results:

    • A significant correlation was found between neutrophil hyperfunction and the HLA-B51 phenotype, irrespective of disease presence.
    • T cells from Behçet's disease patients, but not normal subjects or rheumatoid arthritis patients, proliferated vigorously in response to a specific human HSP-60 peptide (amino acids 336-351).
    • Specific TCR V beta subfamilies were implicated in the antigen-specific proliferation of HSP-responsive T cells, suggesting a role in autoimmunity.

    Conclusions:

    • Recurrent exposure to HSP may break self-tolerance, triggering T cell responses to self- and microbial HSP, producing pro-inflammatory cytokines.
    • Tissue injury in Behçet's disease may result from delayed-type hypersensitivity, macrophage activation, and neutrophil recruitment.
    • A novel multistep molecular mimicry mechanism, involving bacterial antigens activating T cells primed by self-HSP peptides, may induce or exacerbate Behçet's disease, leading to autoreactive T cell selection.