Journal of Leukocyte Biology
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Originally published online as doi:10.1189/jlb.1102525 on July 1, 2003

Published online before print July 1, 2003
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(Journal of Leukocyte Biology. 2003;74:611-619.)
© 2003 by Society for Leukocyte Biology

Activation of Rac2 and Cdc42 on Fc and complement receptor ligation in human neutrophils

Maria Forsberg*, Pia Druid{dagger}, Limin Zheng*, Olle Stendahl* and Eva Särndahl{dagger},1

Departments of
{dagger} Cell Biology and
* Medical Microbiology, Faculty of Health Sciences, Linköping University, Sweden

1Correspondence: Department of Cell Biology, Faculty of Health Sciences, Linköping University, SE- 581 85 Linköping, Sweden. E-mail: eva.sarndahl{at}ibk.liu.se

Phagocytosis is a complex process engaging a concerted action of signal-transduction cascades that leads to ingestion, subsequent phagolysosome fusion, and oxidative activation. We have previously shown that in human neutrophils, C3bi-mediated phagocytosis elicits a significant oxidative response, suggesting that activation of the small GTPase Rac is involved in this process. This is contradictory to macrophages, where only Fc receptor for immunoglobulin G (Fc{gamma}R)-mediated activation is Rac-dependent. The present study shows that engagement of the complement receptor 3 (CR3) and Fc{gamma}R and CR3- and Fc{gamma}R-mediated phagocytosis activates Rac, as well as Cdc42. Furthermore, following receptor-engagement of the CR3 or Fc{gamma}Rs, a downstream target of these small GTPases, p21-activated kinase, becomes phosphorylated, and Rac2 is translocated to the membrane fraction. Using the methyltransferase inhibitors N-acetyl-S-farnesyl-L-cysteine and N-acetyl-S-geranylgeranyl-L-cysteine, we found that the phagocytic uptake of bacteria was not Rac2- or Cdc42-dependent, whereas the oxidative activation was decreased. In conclusion, our results indicate that in neutrophils, Rac2 and Cdc42 are involved in FcR- and CR3-induced activation and for properly functioning signal transduction involved in the generation of oxygen radicals.

Key Words: Rho–GTPases • phagocytosis • NADPH oxidase • ß2 integrin • leukocytes




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