Overexpression of vascular permeability factor (VPF/VEGF) and its endothelial cell receptors in delayed hypersensitivity skin reactions.

摘要: Delayed hypersensitivity (DH) is a T cell-mediated form of immune response characterized by predominantly perivascular, mononuclear cell infiltrate. The venules in DH reactions are hyperpermeable to plasma proteins, leading extravasation fibrinogen and its extravascular clotting fibrin gel that promotes induration angiogenesis. mechanisms responsible for microvascular hyperpermeability unknown. Recently, cytokine named vascular permeability factor (VPF, also known as endothelial growth or VEGF) has been implicated the chronic angiogenesis solid ascites tumors, healing wounds, rheumatoid arthritis, psoriasis. These findings suggested VPF/VEGF might have role pathogenesis DH. Two model systems were studied: allergic contact dermatitis poison ivy human volunteers classical tuberculin rats. In both, situ hybridization revealed mRNAs encoding strikingly overexpressed keratinocytes epidermis; scattered cells infiltrating dermis mRNA, greater extent rat than reactions. reactions, two receptors, flt-1 KDR, overexpressed. Abundant deposition both models confirmed dermal microvessels indeed fibrinogen. results implicate potentially important mediator immunity provide further evidence products epithelial may regulate inflammatory response.