The Journal of Immunology, Vol 143, Issue 7 2295-2301, Copyright © 1989 by American Association of Immunologists

ARTICLES

The effect of IFN-gamma and colony-stimulating factors on the expression of neutrophil cell membrane receptors

AM Buckle and N Hogg
Macrophage Laboratory, Imperial Cancer Research Fund, London, England.

The recombinant cytokines IFN-gamma, granulocyte-macrophage (GM)-CSF, and granulocyte (G)-CSF are all known to affect the function of neutrophils. We have investigated their ability to alter the surface expression of neutrophil Fc gamma R and CR. FcRI, formerly considered to be mononuclear phagocyte specific, was found on a variable percentage of neutrophils after 12 h of tissue culture. These levels could be readily enhanced by IFN-gamma at 0.5 U/ml suggesting that neutrophil FcRI is extremely sensitive IFN-gamma. In addition, membrane expression of FcRIII, the most abundant receptor of neutrophils, could also be increased by IFN-gamma and by GM-CSF and G-CSF. However, the opposite effect was observed in samples in which the initial levels of FcRIII were high. In these situations IFN-gamma and GM-CSF caused a decrease in receptor expression. No consistent alterations were found in the levels of FcRII. Cytokine-induced increases in both FcRI and FcRIII were not evident within the first hour of treatment suggesting that these molecules are not available in an intracellular compartment but must be newly synthesized. In contrast, the CR, CR1 and CR3, could be rapidly induced by GM-CSF indicating that this cytokine causes the mobilization of preformed molecules to the membrane. G-CSF and IFN- gamma did not alter the expression of CR1 and CR3. Thus, the very different effects of IFN-gamma, GM-CSF, and G-CSF suggest that the neutrophil functional profile will be distinctively affected by exposure to each of these cytokines.

This article has been cited by other articles:

				K A Brown, S M Lewis, T A Hill, M G Macey, D A McCarthey, V A Grant, and D F Treacher Leucodepletion and the interaction of polymorphonuclear cells with endothelium in systemic inflammatory response syndrome Perfusion, January 1, 2001; 16(1_suppl): 75 - 83. [Abstract] [PDF]

				R. Menegazzi, S. Busetto, R. Cramer, P. Dri, and P. Patriarca Role of Intracellular Chloride in the Reversible Activation of Neutrophil {beta}2 Integrins: A Lesson from TNF Stimulation J. Immunol., October 15, 2000; 165(8): 4606 - 4614. [Abstract] [Full Text] [PDF]

				E. M. B. Raeder, P. J. Mansfield, V. Hinkovska-Galcheva, J. A. Shayman, and L. A. Boxer Syk Activation Initiates Downstream Signaling Events During Human Polymorphonuclear Leukocyte Phagocytosis J. Immunol., December 15, 1999; 163(12): 6785 - 6793. [Abstract] [Full Text] [PDF]

				D. A. Moulding, C. Walter, C. A. Hart, and S. W. Edwards Effects of Staphylococcal Enterotoxins on Human Neutrophil Functions and Apoptosis Infect. Immun., May 1, 1999; 67(5): 2312 - 2318. [Abstract] [Full Text] [PDF]

				R. Menegazzi, S. Busetto, E. Decleva, R. Cramer, P. Dri, and P. Patriarca Triggering of Chloride Ion Efflux from Human Neutrophils as a Novel Function of Leukocyte {beta}2 Integrins: Relationship with Spreading and Activation of the Respiratory Burst J. Immunol., January 1, 1999; 162(1): 423 - 434. [Abstract] [Full Text] [PDF]

				S. G. Ericson, Y. Zhao, H. Gao, K. L. Miller, L. F. Gibson, J. P. Lynch, and K. S. Landreth Interleukin-6 Production by Human Neutrophils After Fc-Receptor Cross-Linking or Exposure to Granulocyte Colony-Stimulating Factor Blood, March 15, 1998; 91(6): 2099 - 2107. [Abstract] [Full Text] [PDF]

				E. Fadlon, S. Vordermeier, T. C. Pearson, A. R. Mire-Sluis, D. C. Dumonde, J. Phillips, K. Fishlock, and K. Alun Brown Blood Polymorphonuclear Leukocytes From the Majority of Sickle Cell Patients in the Crisis Phase of the Disease Show Enhanced Adhesion to Vascular Endothelium and Increased Expression of CD64 Blood, January 1, 1998; 91(1): 266 - 274. [Abstract] [Full Text] [PDF]