1. ¹ Divisions of Biochemistry and Molecular Biology, John Curtin School of Medical Research, Australian National University, Acton, Australian Capital Territory, Australia
2. ² Division of Immunology and Cell Biology, John Curtin School of Medical Research, Australian National University, Acton, Australian Capital Territory, Australia
3. ³ Division of Pulmonary Medicine, Allergy, and Clinical Immunology, Department of Pediatrics, Childrens Hospital, Medical Center, Cincinnati, Ohio, USA

Correspondence: PS Foster, Division of Biochemistry and Molecular Biology, John Curtin School of Medical Research, Australian National University, Acton, ACT 0200, Australia. Email: <Paul.Foster@anu.edu.au>

Received 15 June 1998; Accepted 15 June 1998.

Abstract

Airway inflammation is central to the pathogenesis of allergic asthma, and molecules that mediate this process obviously represent targets for therapy. In the present article, we discuss our experiments, which point to CD4⁺ T cells and IL-5-driven eosinophilia as potential targets for the relief of bronchial hyperractivity in late-phase asthma.