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Blood, 1 February 2006, Vol. 107, No. 3, pp. 1178-1183.
Prepublished online as a Blood First Edition Paper on October 13, 2005; DOI 10.1182/blood-2005-07-2692.
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PHAGOCYTES
Interaction between integrin  9 1 and vascular cell adhesion molecule-1 (VCAM-1) inhibits neutrophil apoptosis
Ewan A. Ross,
Mike R. Douglas,
See Heng Wong,
Emma J. Ross,
S. John Curnow,
Gerard B. Nash,
Ed Rainger,
Dagmar Scheel-Toellner,
Janet M. Lord,
Mike Salmon, and
Christopher D. Buckley
From the Division of Immunity and Infection, Division of Neurosciences, Division of Medical Sciences, Medical Research Council (MRC) Centre for Immune Regulation, Institute for Biomedical Research, University of Birmingham, United Kingdom.
According to the prevailing paradigm, neutrophils are short-lived cells that undergo spontaneous apoptosis within 24 hours of their release from the bone marrow. However, neutrophil survival can be significantly prolonged within inflamed tissue by cytokines, inflammatory mediators, and hypoxia. During screening experiments aimed at identifying the effect of the adhesive microenvironment on neutrophil survival, we found that VCAM-1 (CD106) was able to delay both spontaneous and Fas-induced apoptosis. VCAM-1-mediated survival was as efficient as that induced by the cytokine IFN- and provided an additive, increased delay in apoptosis when given in combination with IFN-. VCAM-1 delivered its antiapoptotic effect through binding the integrin  91. The 91 signaling pathway shares significant features with the IFN- survival signaling pathway, requiring PI3 kinase, NF- B activation, as well as de novo protein synthesis, but the kinetics of NF-B activation by VCAM-1 were slower and more sustained compared with IFN-. This study demonstrates a novel functional role for 91 in neutrophil biology and suggests that adhesive signaling pathways provide an important extrinsic checkpoint for the resolution of inflammatory responses in tissues.
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[Abstract]
[Full Text]
[PDF]
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