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A CD1d-dependent antagonist inhibits the activation of iNKT cells and prevents development of allergen-induced airway hyperreactivity

¹ Division of Immunology, Children’s Hospital, Harvard Medical School, 1 Blackfan Circle, Boston, MA, 02115, ² Massachusetts General Hospital, Harvard Medical School, 65 Landsdowne St., Cambridge, MA, 02139

Abstract

The prevalence of asthma continues to increase and its optimal treatment remains a significant therapeutic challenge. Recently, CD1d-restricted iNKT cells were found to play a critical role in the induction of airway hyperreactivity (AHR) in rodents and are associated with severe peristent asthma in humans. To test whether iNKT cell-targeted therapy could be used to treat allergen-induced airway hyperreactivity disease, mice sensitized with ovalbumin were treated with a CD1d-binding lipid antagonist, DPPE-PEG. A single dose of DPPE-PEG prevented the development of AHR and pulmonary infiltrates after ovalbumin challenge, but not the development of ovalbumin-specific Th2 responses. Because iNKT cells play a critical role in the development of AHR, the inhibition of iNKT activation by DPPE-PEG suggests a novel therapy for iNKT cell-mediated diseases such as asthma.

This Article Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Akbari, O. Articles by Wilson, S. B. PubMed Articles by Akbari, O. Articles by Wilson, S. B.