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GM-CSF induces human neutrophil IgA-mediated phagocytosis by an IgA Fc receptor activation mechanism
Abstract
Immunoglobulin A is the primary immunoglobulin isotype in tears, saliva, breast milk and other mucosal secretions, constituting between 6% and 15% of the total serum immunoglobulins. Human peripheral blood neutrophils have IgA receptors, but these cells do not normally participate in IgA-mediated phagocytosis. The haematopoietic factors granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) prime neutrophils to be more responsive to a variety of stimuli. We therefore studied their effect on IgA-mediated phagocytosis. GM-CSF and G-CSF both induce a change from low to high-affinity neutrophil IgA Fc crystallizable fragment receptors within 30 min; a change which is associated with the development of IgA-mediated phagocytosis. Human IL-3, which does not affect neutrophil function, is inactive in this system. These results define a new mechanism for CSF-augmented host defence whereby neutrophil function can be modulated by CSF-mediated IgA Fc receptor activation.
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“Short-term in vitro exposure to GM-CSF, so-called priming, favors functional responses of neutrophils [30,57–59], while long-term stimulation with GM-CSF alters the transcriptional profile of neutrophils [28,38].”
From Nascent RHOH acts as a molecular brake on actomyosin-mediated effector functions of inflammatory neutrophils (2022) · cites this paper as [58]
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Research works printed but not linked: 15
- Conley, M. E. & Delacroix, D. L. Ann. intern. Med. 106, 892–899 (1987). · DOI
- Weisbart, R. H., Golde, D. W., Clark, S. C., Wong, G. C. & Gasson, J. C. Nature 314, 361–363 (1985). · DOI
- Weisbart, R. H., Kwan, L., Golde, D. W. & Gasson, J. C. Blood 69, 18–21 (1987). · DOI
- Lopez, A. F. et al. J. Immunol. 131, 2983–2988 (1981). · DOI
- Klebanoff, D. J. & Clark, R. A. The Neutrophil: Function and Clinical Disorders (North-Holland, Amsterdam, New York, Oxford, 1978).
- Quie, P. G., Messner, R. P. & Williams, R. C. Jr J. exp. Med. 128, 553–570 (1968). · DOI
- Wilson, J. D. J. Immunol. 108, 726–730 (1972). · DOI
- Zipursky, A., Brown, E. J. & Bienenstock, J. Proc. Soc. exp. Biol. (N. Y.) 142, 181–184 (1973). · DOI
- Fanger, M. W., Goldstine, S. N. & Shen, L. Molec. Immunol 20, 1019–1027 (1983). · DOI
- Weisbart, R. H., Golde, D. W. & Gasson, J. C. J. Immunol. 137, 3584–3587 (1986). · DOI
- Gasson, J. C., Kaufman, S. E., Weisbart, R. H., Tomonaga, M. & Golde, D. W. Proc. natn. Acad. Sci. U.S.A. 83, 669–673 (1986). · DOI
- Calvo, J. C., Radicella, J. P. & Charreau, E. H. Biochem. J. 212, 259–264 (1983). · DOI
- Tagliabue, A. et al. J. Immunol. 133, 988–992 (1984). · DOI
- Tagliabue, A., Villa, L., Boraschi, K., Peri, G., deGori, V. & Nencioni, L. J. Immunol. 135, 4178–4182 (1985). · DOI
- Maliszewski, C. R., Shen, L. & Fanger, M. W. J. Immunol. 135, 3878–3881 (1985). · DOI
Cited by
Wodnar-Filipowicz, A., Heusser, C. H., & Moroni, C. (1989) · Nature · doi:10.1038/339150a0 · Cited by 480
Fetissov, S. O., Hamze Sinno, M., Coëffier, M., Bole-Feysot, C., Ducrotté, P., Hökfelt, T., & Déchelotte, P. (2008) · Nutrition · doi:10.1016/j.nut.2007.12.006 · Cited by 175
Peng, S., Stojkov, D., Gao, J., Oberson, K., Latzin, P., Casaulta, C., Yousefi, S., & Simon, H.-U. (2022) · PLOS Biology · doi:10.1371/journal.pbio.3001794 · Cited by 15
Metadata
- Authors
- Weisbart, R. H., Kacena, A., Schuh, A., & Golde, D. W.
- Venue
- Nature
- Published
- 1988-04
- Volume
- 332
- Issue
- 6165
- Pages
- 647-648
- ISSN
- 0028-0836
- 1476-4687
- Cited by
- 160
- References
- 0
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
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