Hyperreactivity of neutrophils and abnormal T cell homeostasis: a new insight for pathogenesis of Behçet's disease

Int Rev Immunol. 1997;14(1):11-9. doi: 10.3109/08830189709116841.


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 gamma delta T cells and alpha beta 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 gamma delta T cells and alpha beta 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.

Publication types

  • Review

MeSH terms

  • Animals
  • Behcet Syndrome / etiology*
  • Behcet Syndrome / genetics
  • Behcet Syndrome / immunology*
  • HLA-B Antigens / genetics
  • HLA-B51 Antigen
  • Homeostasis
  • Humans
  • Immunity, Mucosal
  • Lymphocyte Activation
  • Mice
  • Mice, Transgenic
  • Neutrophils / immunology*
  • Neutrophils / metabolism
  • Receptors, Antigen, T-Cell, gamma-delta / metabolism
  • Superoxides / metabolism
  • T-Lymphocytes / immunology*


  • HLA-B Antigens
  • HLA-B51 Antigen
  • Receptors, Antigen, T-Cell, gamma-delta
  • Superoxides