Abstract
Chronic spontaneous urticaria (CSU) skin lesions demonstrate evidence of mast cell degranulation and infiltration by basophils, eosinophils, and T lymphocytes. The pathways for leukocyte recruitment and activation remain unknown. We previously reported that CSU basophils and eosinophils demonstrate altered CRTH2 expression and function that improved with CRTH2 antagonist therapy. Therefore, we sought to determine whether CSU patients possess dysregulated production of prostaglandin D2 (PGD2), a primary CRTH2 ligand, by examining skin and urine specimens.
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