PL EN


Preferences help
enabled [disable] Abstract
Number of results
2000 | 48 | 5 | 487-496
Article title

Suppression of mast cell activation by glucocorticoid

Title variants
Languages of publication
EN
Abstracts
EN
Mast cells play a critical role in allergic diseases. When mast cells are activated by cross-linking of their high affinity IgE receptors by the antigen and IgE antibodies, release of chemical mediators is followed by secretion of multiple cytokines. We report that IL-3-dependent mucosal-type mast cells undergo apoptosis when IL-3 is withdrawn. In addition, cross-linking of high affinityIgE receptors prevents apoptosis of mast cells by paractine mechanisms, producing IL-3, IL-4 and granulocyte/macrophage colony-stimulating factor (GM-CSF). However, the secretion of endogenous growth factors are not enough for cell survival, whereas IL-4 induces cell aggregation by expressing adhesion molecules such as leukocyte function-associated antigen 1 (LFA-1), and makes it reactive to endogenous growth factors by contact cell to cell interaction. On the other hand, dexamethazone down-regulates the expression of intracellular adhesion molecule 1 (ICAM-1) and IL-4 in activated mast cells, by which the self-aggregation of mast cells is inhibited and poptosis is induced. Thus, glucocorticoids suppress mast cell survival by inhibiting IL-4 production and expression of adhesion molecules.
Publisher

Year
Volume
48
Issue
5
Pages
487-496
Physical description
Contributors
author
author
References
Document Type
REVIEW
Publication order reference
H. Yoshikawa, Department of Parasitology and Immunology, Yamanashi Medical University, 1110 Shimokato, Tamaho-cho, Yamanashi 409-3898, Japan
Identifiers
YADDA identifier
bwmeta1.element.element-from-psjc-9a609e61-b9ba-3442-952c-87414434414f
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.