Suppression of mast cell activation by glucocorticoid

• Authors: H. Yoshikawa , K. Tasaka
• 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 We report that IL-3-dependent mucosal-type mast cells undergo apoptosis when IL-3 is withdrawn.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.

Keywords

EN

ADHESION MOLECULE; ALLERGY; CYTOKINE; GLUCOCORTICOID; MAST CELL

Discipline

• IMMUNOLOGY: IMMUNOLOGY

• Publisher: Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences
• Journal: Archivum Immunologiae et Therapiae Experimentalis
• Year: 2000
• Volume: 48
• Issue: 5
• Pages: 487-496

Contributors

author

H. Yoshikawa

author

K. Tasaka

• Document Type: REVIEW
• Publication order reference: H. Yoshikawa, Department of Parasitology and Immunology, Yamanashi Medical University, 1110 Shimokato, Tamaho-cho, Yamanashi 409-3898, Japan