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on apoptosis of human neutrophils
* Central Laboratory of the Netherlands Blood Transfusion Service and Laboratory for Experimental and Clinical Immunology, Academic Medical Center, University of Amsterdam; and
Departments of Pediatrics and
Pathology, Academic Medical Center, University of Amsterdam, The Netherlands
Correspondence: Taco W. Kuijpers, M.D., Ph.D., CLB, Dept. IHE, F116, Plesmanlaan 125, 1066 CX Amsterdam, The Netherlands. E-mail: T_Kuijpers{at}CLB.NL
Apoptosis of neutrophils is a key mechanism to control the intensity of
the acute inflammatory response. Previously, the cytokine tumor
necrosis factor 
(TNF-) was reported by some to have
pro-apoptotic and by others to have anti-apoptotic effects on
neutrophils. The aim of this study was to explain these contradictory
results. We found that TNF- at low concentrations strongly decreased
apoptosis of neutrophils. However, at higher concentrations, TNF-
lost its protective effects, and also reversed the protective effects
of interferon-
(IFN-) and granulocyte-macrophage
colony-stimulating factor (GM-CSF). This pro-apoptotic effect of
TNF- was blocked by anti-CD11b and was absent in neutrophils from
patients with chronic granulomatous disease, which cannot produce toxic
oxygen metabolites. Under these circumstances, we found that TNF-
retained its anti-apoptotic effects even at high concentrations. In
conclusion, the protective effects against apoptosis of IFN-,
GM-CSF, and TNF- itself are overruled when the concentration of
TNF- is high enough to produce a respiratory burst. These dual,
concentration-dependent effects of TNF- provide an explanation for
previous controversial reports and support a dominant role for TNF-
in neutrophil apoptosis.
Key Words: leukocyte adhesion deficiency • chronic granulomatous disease • granulocyte-macrophage colony-stimulating factor • interferon- • CD11b/CD18
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