Hyperreactivity of Neutrophils and Abnormal T Cell Homeostasis: a New Insight for Pathogenesis of Behçet's Disease

Abstract

Neutrophil hyperfunction of Behçet's disease is in part regulated by genetical factors, especially related to HLA-B51 genes and by immunological abnormalities. Regarding the latter points, Behçet's disease worsens with abnormal regulation by γδ T cells and αβ T cells. Indeed, our own studies and those of other laboratories suggest that human heat shock protein may be one of the triggering factors for activation of both the γδ T cells and αβ T cells. These activated T cells may produce proinflammatory and/or inflammatory cytokines, and lead to tissue injury possibly via delayed-type hypersensitivity reaction, macrophage activation, and activation and/or recruitment of neutrophils. Here we discuss the crosstalk between the immune system and neutrophils in this disease.

Key Words:

• Neutrophils
• HLA-B51
• Transgenic mice
• γδ T cells
• αβ T cells
• Heat shock protein