Neutrophils are important effector cells of the innate immune system that are capable of responding rapidly to infectious organisms to which to the immune system may be naive. However, in certain circumstances their actions can be inappropriate or ineffective. A lack of effective neutrophil function increases the number or persistence of infections. This is well illustrated by inherited disorders that impair neutrophil effector function. In chronic granulomatous disease, deficient activity of NADPH oxidase (usually the membrane-bound gp91 subunit) results in the absence of a respiratory burst and the production of reactive oxygen species necessary for microbial killing, resulting in frequent infection. Defects in the leucocyte adhesion molecules (2 integrins or selectin molecules) necessary for neutrophil interaction with endothelium lead to poor recruitment to sites of infection and hence an inability to effectively fight infection [1]. In some patients the opposite situation occurs, where inappropriate and prolonged neutrophil activation leads to tissue damage. There is evidence that in the presence of anti-neutrophil cytoplasmic antibodies (ANCA), which develop in some forms of autoimmune vasculitis, neutrophils adhere to endothelium and undergo a respiratory burst leading to endothelial damage. Dysregulated apoptosis and inefficient removal of these neutrophils by macrophages leads to chronic inflammation and organ damage [2–4]. Such events contribute to the tissue injury associated with the inflammatory disease. Therefore, a potential goal of therapy for diseases involving aberrant neutrophil function in the context of inflammation and autoimmunity would be to manipulate the function of the neutrophil in vivo. There are several places along that the chain of events, starting with neutrophil activation and ending in the release of reactive oxygen species, that may be amenable to intervention: � Preventing neutrophil recruitment across vascular endothelium. � Down-regulating neutrophil activation at the level of receptormediated events or intracellular signalling pathways. � Targeting cytotoxic products of neutrophil activation. � Manipulating neutrophil life span and/or promoting nonphlogistic removal.