Hyperreactivity of neutrophils and abnormal T cell homeostasis: a new insight for pathogenesis of Behçet's disease.
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.
Yamashita
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Department of Immunology, St. Marianna University, School of Medicine, Kanagawa, Japan.
D000818:Animals; D001528:Behcet Syndrome / Q000209:etiology* / Q000235:genetics / Q000276:immunology*; D015235:HLA-B Antigens / Q000235:genetics; D059949:HLA-B51 Antigen; D006706:Homeostasis; D006801:Humans; D018928:Immunity, Mucosal; D008213:Lymphocyte Activation; D051379:Mice; D008822:Mice, Transgenic; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology*
D015235:HLA-B Antigens; D059949:HLA-B51 Antigen; D016692:Receptors, Antigen, T-Cell, gamma-delta; D013481:Superoxides