Cited by 160

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GM-CSF induces human neutrophil IgA-mediated phagocytosis by an IgA Fc receptor activation mechanism

Weisbart, R. H., Kacena, A., Schuh, A., Golde, D. W.·1988·Nature

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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Research works printed but not linked: 15

  1. Conley, M. E. & Delacroix, D. L. Ann. intern. Med. 106, 892–899 (1987). · DOI
  2. Weisbart, R. H., Golde, D. W., Clark, S. C., Wong, G. C. & Gasson, J. C. Nature 314, 361–363 (1985). · DOI
  3. Weisbart, R. H., Kwan, L., Golde, D. W. & Gasson, J. C. Blood 69, 18–21 (1987). · DOI
  4. Lopez, A. F. et al. J. Immunol. 131, 2983–2988 (1981). · DOI
  5. Klebanoff, D. J. & Clark, R. A. The Neutrophil: Function and Clinical Disorders (North-Holland, Amsterdam, New York, Oxford, 1978).
  6. Quie, P. G., Messner, R. P. & Williams, R. C. Jr J. exp. Med. 128, 553–570 (1968). · DOI
  7. Wilson, J. D. J. Immunol. 108, 726–730 (1972). · DOI
  8. Zipursky, A., Brown, E. J. & Bienenstock, J. Proc. Soc. exp. Biol. (N. Y.) 142, 181–184 (1973). · DOI
  9. Fanger, M. W., Goldstine, S. N. & Shen, L. Molec. Immunol 20, 1019–1027 (1983). · DOI
  10. Weisbart, R. H., Golde, D. W. & Gasson, J. C. J. Immunol. 137, 3584–3587 (1986). · DOI
  11. 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
  12. Calvo, J. C., Radicella, J. P. & Charreau, E. H. Biochem. J. 212, 259–264 (1983). · DOI
  13. Tagliabue, A. et al. J. Immunol. 133, 988–992 (1984). · DOI
  14. Tagliabue, A., Villa, L., Boraschi, K., Peri, G., deGori, V. & Nencioni, L. J. Immunol. 135, 4178–4182 (1985). · DOI
  15. Maliszewski, C. R., Shen, L. & Fanger, M. W. J. Immunol. 135, 3878–3881 (1985). · DOI

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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

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CoChat. (2026). Citation check: GM-CSF induces human neutrophil IgA-mediated phagocytosis by an IgA Fc receptor activation mechanism. https://app.cochat.ai/papers/10.1038/332647a0
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Weisbart, R. H., Kacena, A., Schuh, A., & Golde, D. W. (1988). GM-CSF induces human neutrophil IgA-mediated phagocytosis by an IgA Fc receptor activation mechanism. Nature. https://doi.org/10.1038/332647a0