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CCR3 antagonists for the treatment of allergy Atopic dermatitis is a pruritic inflammatory skin disease affecting 10% of the population at some time in their life with about 60% of them continuing to have symptoms into adulthood. More than 15 million people have symptoms of the disease in the US alone. This condition often begins in infancy and frequently affects individuals with personal or family history of atopic disease. The majority of infants with atopic dermatitis develop asthma and/or allergic rhinitis later in life. The world market for drugs to treat allergic diseases is a massive £10 billion and is growing at over 10% per annum. New products in current development offer little therapeutic advantage or improved patient compliance over existing therapy. Consequently, there is a clear need for new agents that can modify these diseases by reprogramming the underlying immune processes. Researchers at the Children's Hospital in Boston have recently demonstrated an excellent proof of concept for one immune target. This group has shown that repeated epicutaneous administration of ovalbumin causes eosinophil skin infiltration, local expression of Th2 cytokines, and airway hyperresponsiveness to inhaled antigen. In contrast, eosinophils were absent from the skin of CCR3 knock-out mice. Furthermore, recruitment of eosinophils to lung parenchyma and bronchoalveolar lavage fluid was severely impaired in these mice. Moreover, they failed to develop airway hyperresponsiveness to methacholine following antigen inhalation. These results suggest that CCR3 plays an essential role in eosinophil recruitment to the skin and the lung and in the development of airway hyperresponsiveness. CCR3 antagonists could therefore offer a highly specific mode of targeting atopic dermatitis. Only a handful of CCR3 antagonists have been developed to date and this field clearly holds considerable potential. Link to journal abstract:
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