Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.1008668 on January 15, 2009

Published online before print January 15, 2009
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Buy
Right arrow All Versions of this Article:
jlb.1008668v1
85/4/627    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by MacGlashan, D.
Right arrow Articles by Vilariño, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by MacGlashan, D., Jr.
Right arrow Articles by Vilariño, N.
(Journal of Leukocyte Biology. 2009;85:627-637.)
© 2009 by Society for Leukocyte Biology

Polymerization of actin does not regulate desensitization in human basophils

Donald MacGlashan, Jr.1 and Natalia Vilariño

Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland, USA

1 Correspondence: Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, USA. E-mail: dmacglas{at}jhmi.edu

ABSTRACT

Previous studies have suggested that maintenance of IgE-mediated signaling results from regulation of the activity of signaling complexes by actin polymerization. This process is also hypothesized to be related to desensitization of basophils and mast cells. Recent studies demonstrated that any signaling process dependent on syk or PI-3K activity cannot be a mechanism of desensitization, and in this context, syk and PI-3K inhibitors were found to inhibit actin polymerization. Inhibitors of actin polymerization were tested for their effect on desensitization of human peripheral blood basophils. Latrunculin A, in particular, removed all resting and stimulated f-actin but did not inhibit desensitization. Cytochalasin D and latrunculin A also did not reverse the loss of syk phosphorylation that accompanies desensitization. These results demonstrate that desensitization mechanisms are not dependent on actin polymerization. In this context, it was also shown that progressive immobilization of Fc{epsilon}RI during aggregation was sensitive to syk or actin polymerization inhibition. Therefore, desensitization is also not dependent on receptor immobilization. These studies demonstrate that desensitization is not the result of two signaling pathways once considered relevant to down-regulation of IgE-mediated signaling.

Key Words: signal termination • Fc{epsilon}RI • histamine release