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Rheumatology Advance Access originally published online on December 14, 2004
Rheumatology 2005 44(5):597-601; doi:10.1093/rheumatology/keh507
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© The Author 2004. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

REVIEW

Can neutrophils be manipulated in vivo?

Aims of Therapy/Series Editor: Lorraine Harper

M. D. Morgan, L. Harper, X. Lu, G. Nash, J. Williams and C. O. S. Savage

Renal Immunobiology, Division of Immunity and Infection, The School of Medicine, University of Birmingham, Birmingham, UK.

Correspondence to: C. O. S. Savage, Renal Immunobiology, Division of Immunity and Infection, The School of Medicine, University of Birmingham, Birmingham B15 2TT, UK. E-mail: c.o.s.savage@bham.ac.uk

The first 150 words of the full text of this article appear below.


   Introduction
 
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 (ß2 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 . . . [Full Text of this Article]


   Neutrophil recruitment
 

   Selectins as targets for manipulating neutrophil recruitment
 

   Inhibition via neutrophil integrins or their endothelial ligands
 

   The chemokine receptors CXCR1 and CXCR2 as targets for neutrophil manipulation
 

   Down-regulating neutrophil activation at the level of receptor-mediated events or intracellular signalling pathways
 
Receptor-mediated events
Intracellular signalling pathways

   Targeting cytotoxic products of neutrophil activation
 

   Manipulating neutrophil life span and/or promoting non-phlogistic removal
 

   Summary
 

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