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Inflammation pp 95-107 | Cite as

Suppression of Mast Cell Activation by Glucocorticoid

  • Hideshi Yoshikawa
  • Kachio Tasaka
Chapter
  • 242 Downloads

Abstract

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 We report that IL-3-dependent mucosal-type mast cells undergo apoptosis when IL-3 is withdrawn.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 affinity IgE receptors prevents apoptosis of mast cells by paracrine 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 intracelluar adhesion molecule 1 (ICAM-1) and IL-4 in activated mast cells, by which the self-aggregation of mast cells is inhibited and apoptosis is induced. Thus, glucocorticoids suppress mast cell survival by inhibiting IL-4 production and expression of adhesion molecules.

Key words

allergy mast cell glucocorticoid cytokine adhesion molecule. 

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Copyright information

© Springer Science+Business Media Dordrecht 2001

Authors and Affiliations

  • Hideshi Yoshikawa
    • 1
  • Kachio Tasaka
    • 1
  1. 1.Department of Parasitology and ImmunologyYamanashi Medical UniversityTamaho-cho, YamanashiJapan

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