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Identification of Novel Target Proteins in Th2-Dominated Allergic Inflammatory Responses Using Complementary DNA Representational Difference Analysis and Complementary DNA Microarrays*

Peter C. Groot, PhD; B. Jerden Van Bergenhenegouwen; Frans P. Nijkamp, PhD; Antoon J. M. Van Oosterhout, PhD
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*From the Department of Pharmacology and Pathophysiology, Utrecht Institute of Pharmaceutical Sciences, Utrecht University, Utrecht, Netherlands.

Correspondence to: P. C. Groot, PhD, Department of Pharmacology and Pathophysiology, Utrecht Institute of Pharmaceutical Sciences, Utrecht University, PO Box 80082, 3508 TB Utrecht, Netherlands; e-mail:P.C.Groot@pharm.uu.nl



Chest. 2002;121(3_suppl):77S-78S. doi:10.1378/chest.121.3_suppl.77S-a
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Patients with allergic asthma are characterized by aberrant immune responses to environmental allergens leading to eosinophilic airway inflammation and hyperresponsiveness. The activation of allergen-specific T-helper type 2 (Th2) lymphocytes, which produce a limited set of cytokines including interleukin (IL)-4 and IL-5, plays a crucial role in the initiation and progression of allergic asthma. Currently, glucocorticoids are the most effective drugs in the treatment of patients with asthma to reduce the inflammatory component and hyperresponsiveness, but they are not very selective and patients can be refractory or become insensitive to them. Novel drug targets that modulate or inactivate disease-inducing Th2 lymphocytes may prove to be superior and more selective. Th2 lymphocytes appear to be generated in the lung-draining lymph nodes, after which they migrate to the lung tissue.

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