IgE-Dependent Release of Inflammatory Mediators from Hamster Mast Cells in Vitro
The release of mediators from mast cells is an essential step in immediate hypersensitivity reactions and also appears to play a significant role in delayed hypersensitivity and some forms of complement mediated reactions (1). Mediator release from rat or human mast cells can be provoked by antigen-IgE interactions on the surface of cells, by C3a or C5a anaphylatoxins, by bradykinin, by basic lysosomal proteins from neutrophils, by certain lymphokines and by a variety of other molecules (1–4). Preformed molecules such as histamine and newly formed molecules such as slow reacting substance-A (SRS-A) and prostaglandin D2 (PGD2) are released which exert potent regulatory influences on tissue function in areas of mast cell secretion. In addition to roles in the effector arms of immune and non-specific inflammation, recent evidence indicates that mast cell mediators may exert important regulatory influences on the evolution of immune responses (5). While the precise roles of mast cells in these immunologic events are not entirely clear, it seems likely that important roles will be delineated in several areas of immune function.
KeywordsMast Cell Apparent Molecular Weight Mediator Release Human Mast Cell Mast Cell Secretion
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