Abstract
Background: Receptors for vasoactive intestinal polypeptide (VIP) have recently been suggested to play a key role in immunomodulation with genetically modified mice. However, it is not known whether changes in receptor gene regulation are involved in the pathogenesis of human immune disorders. Objective: We studied the expression of VPAC2 in acute lesions of the human immune disease atopic dermatitis. Methods: By using nonradioactive in situ hybridization, quantitative immunohistochemistry, RT-PCR, and gene array studies, the expression status of VPAC2 was assessed in atopic dermatitis and control tissues and in the human mast cell line HMC-1. Results: In situ hybridization and immunohistochemistry demonstrated VPAC2 mRNA and protein expression in human mast cells surrounded by VIP positive nerve fibers. Gene array experiments and RT-PCR studies showed high levels of VPAC2 mRNA expression in mast cells that were increased compared to other receptors such as VPAC1 or VIP in the human mast cell line HMC-1. Stimulation of HMC-1 cells led to a downregulation of VPAC2. Similarly, quantitative immunohistochemistry for VPAC2 in acute atopic dermatitis lesions showed a significantly decreased VPAC2 immunoreactivity in mast cells. Conclusion: The downregulation of VPAC2 in human mast cells in acute lesions of atopic dermatitis suggests a role of this G-protein;coupled receptor in the pathophysiology of the disease. (J Allergy Clin Immunol 2003;111:1099-105.)
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