Negative signals from FcepsilonRI engagement attenuate mast cell functions.
Mast cells have long been recognized as the critical tissue-based effector cells in IgE-mediated allergic diseases. Ligation of the high-affinity receptor for IgE (FcepsilonRI), constitutively expressed on mast cells, promotes cell activation and immediate release and production of pro-inflammatory mediators. Besides these positive signals, FcepsilonRI aggregation has recently been understood to generate negative intracellular signals capable of limiting mast cell functional responses. This review is aimed at providing a summary of the mechanisms through which FcepsilonRI engagement can generate negative signals and regulate mast-cell function. Similar mechanisms are employed by other receptors expressed by immune cells, such as T cell and B cell receptors, pointing to a general concept in negative immunoreceptor signaling.
Department of Experimental Medicine, University "La Sapienza", Viale Regina Elena 324, 00161, Rome, Italy.
Rosa
R
Molfetta
Giovanna
G
Peruzzi
Angela
A
Santoni
Rossella
R
Paolini
D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D000818:Animals; D025461:Feedback, Physiological; D006801:Humans; D006967:Hypersensitivity / Q000378:metabolism; D007073:Immunoglobulin E / Q000378:metabolism*; D008407:Mast Cells / Q000201:enzymology / Q000378:metabolism*; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism; D021122:Protein Subunits; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D011940:Receptor Aggregation; D017455:Receptors, IgE / Q000378:metabolism*; D015398:Signal Transduction
D048868:Adaptor Proteins, Signal Transducing; D021122:Protein Subunits; D017455:Receptors, IgE; D007073:Immunoglobulin E; D011505:Protein-Tyrosine Kinases; D010744:Phosphoric Monoester Hydrolases