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Abstract

Introduction

Resolution of inflammation in asthma is typically thought of as a passive phenomenon in which proinflammatory Th2-type cytokines wane after the initial trigger. We hypothesized that active mechanisms, including anti-inflammatory cytokines and proapoptotic factors, contribute to this process. Fas Ligand (FasL) expression was particularly interesting since important effector cells in asthma (e.g. eosinophils and T helper cells) are Fas-sensitive.

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