Review Article
Signaling through the high affinity IgE receptor and conditions able to modify IgE-antigen responsiveness of mast cells
Claudia Gonzalez-Espinosa, Jaciel Medina-Tamayo,
Elizabeth Sanchez-Miranda,
Juan Pablo Benitez-Garrido,
Alejandro Martin Avila-Hernandez,
Alejandro Padilla,
Jonathan Garcia-Roman,
Jaciel Medina-Tamayo
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorElizabeth Sanchez-Miranda
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorJuan Pablo Benitez-Garrido
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorAlejandro Martin Avila-Hernandez
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorAlejandro Padilla
Immunology Department, Faculty of Medicine, National Autonomous University of Mexico, Mexico City, Mexico
Search for more papers by this authorJonathan Garcia-Roman
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorClaudia Gonzalez-Espinosa, Jaciel Medina-Tamayo,
Elizabeth Sanchez-Miranda,
Juan Pablo Benitez-Garrido,
Alejandro Martin Avila-Hernandez,
Alejandro Padilla,
Jonathan Garcia-Roman,
Jaciel Medina-Tamayo
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorElizabeth Sanchez-Miranda
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorJuan Pablo Benitez-Garrido
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorAlejandro Martin Avila-Hernandez
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorAlejandro Padilla
Immunology Department, Faculty of Medicine, National Autonomous University of Mexico, Mexico City, Mexico
Search for more papers by this authorJonathan Garcia-Roman
Pharmacobiology Department, Center for Research and Advanced Studies (CINVESTAV), South Campus, National Autonomous University of Mexico, Mexico City, Mexico. Fax: +55 50 612863
Search for more papers by this authorAbstract
Signaling through the high affinity receptor for IgE (FcεRI) on mast cells comprises an intricate network of protein-protein modifications and interactions leading to mast cell degranulation, lipid-derived mediator production and cytokine release. Depending on the tissue where mast cells are activated, mediator release can induce distinct allergy symptoms. FcεRI receptor mainly couples to at least two Src family kinases (Lyn and Fyn), which are responsible for the initiation of the signaling cascade. Distinct membrane bound adapters couple the initial signal to the formation of particular multi-molecular complexes that, in turn, will mediate a specific final response. In this review we summarize the molecular mechanisms initiated by the FcεRI receptor on mast cells that have been involved in cytokine expression. At the same time, some conditions where the main signal transduction mechanism is modified will be analyzed in order to understand how locally produced mediators could alter IgE-antigen-induced allergic responses.
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