Abstract

Recruitment of T cells to the airways is crucial in the pathogenesis of asthma, and it is thought to be mediated mainly by peptide chemokines. By contrast, lipid mediators such as leukotrienes and prostaglandins have classically been thought to contribute to asthma pathogenesis by other mechanisms. However, as we discuss here, the recent molecular identification of leukotriene and prostaglandin receptors, as well as the generation of mice that are genetically deficient in them, has revealed that two of these lipids — leukotriene B₄ and prostaglandin D₂ — also direct T-cell migration and seem to cooperate with chemokines in a non-redundant, sequential manner to recruit T cells to the airways in asthma.

Author affiliations

1. Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Building 149-8301, 13th Street, Charlestown, Massachusetts 02129, United States.
2. Pulmonary and Critical Care Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, United States.

Correspondence to: Andrew D. Luster¹ Email: aluster@partners.org

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