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Microfilaments make mast cells migrate (rather than degranulate)
Author(s) -
Huber Michael
Publication year - 2013
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.201343706
Subject(s) - degranulation , microbiology and biotechnology , chemotaxis , stem cell factor , biology , mast cell , secretion , immunoglobulin e , immunology , receptor , stem cell , haematopoiesis , antibody , biochemistry
Expression of the high‐affinity receptor for I g E ( F cε RI ) provides mast cells with the ability to react in a proinflammatory manner to antigens ( A gs). In particular, the immediate secretion of preformed mediators from secretory lysosomes (degranulation) is typical for F cε RI ‐mediated mast cell activation. In addition to the F cε RI , the stem cell factor receptor, KIT , is expressed at high levels on the surface of mast cells. KIT activation controls mast cell differentiation and survival in vivo and potently stimulates the chemotaxis of these cells. Although F cε RI and KIT initiate many of the same early signaling events in mast cells, F cε RI activation results in potent degranulation and a poor chemotactic response while KIT activation triggers very little degranulation and a strong chemotactic response. Novel data published in this issue of the E uropean J ournal of I mmunology [ S mrž et al. Eur. J. Immunol. 2013. 43: 1873‐1882] demonstrate that actin de‐ and repolymerization, involved in both degranulation and chemotaxis, make all the difference: Pharmacological suppression of F ‐actin formation converts activated KIT into a strong degranulator. The possible implications for mast cell physiology and pathophysiology are discussed in this C ommentary.