title: Vesicular trafficking and signaling for cytokine and chemokine secretion in mast cells.
abstract: Upon activation mast cells (MCs) secrete numerous inflammatory compounds stored in their cytoplasmic secretory granules by a process called anaphylactic degranulation, which is responsible for type I hypersensitivity responses. Prestored mediators include histamine and MC proteases but also some cytokines and growth factors making them available within minutes for a maximal biological effect. Degranulation is followed by the de novo synthesis of lipid mediators such as prostaglandins and leukotrienes as well as a vast array of cytokines, chemokines, and growth factors, which are responsible for late phase inflammatory responses. While lipid mediators diffuse freely out of the cell through lipid bilayers, both anaphylactic degranulation and secretion of cytokines, chemokines, and growth factors depends on highly regulated vesicular trafficking steps that occur along the secretory pathway starting with the translocation of proteins to the endoplasmic reticulum. Vesicular trafficking in MCs also intersects with endocytic routes, notably to form specialized cytoplasmic granules called secretory lysosomes. Some of the mediators like histamine reach granules via specific vesicular monoamine transporters directly from the cytoplasm. In this review, we try to summarize the available data on granule biogenesis and signaling events that coordinate the complex steps that lead to the release of the inflammatory mediators from the various vesicular carriers in MCs.
authors.affiliation: INSERM UMRS 1149 , Paris , France ; CNRS ERL8252 , Paris , France ; Université Paris Diderot, Sorbonne Paris Cité, Laboratoire d'excellence INFLAMEX , Paris , France.
authors.forename: Ulrich
authors.initials: U
authors.lastname: Blank
authors.affiliation: INSERM UMRS 1149 , Paris , France ; CNRS ERL8252 , Paris , France ; Université Paris Diderot, Sorbonne Paris Cité, Laboratoire d'excellence INFLAMEX , Paris , France.
authors.forename: Iris Karina
authors.initials: IK
authors.lastname: Madera-Salcedo
authors.affiliation: INSERM UMRS 1149 , Paris , France ; CNRS ERL8252 , Paris , France ; Université Paris Diderot, Sorbonne Paris Cité, Laboratoire d'excellence INFLAMEX , Paris , France.
authors.forename: Luca
authors.initials: L
authors.lastname: Danelli
authors.affiliation: INSERM UMRS 1149 , Paris , France ; CNRS ERL8252 , Paris , France ; Université Paris Diderot, Sorbonne Paris Cité, Laboratoire d'excellence INFLAMEX , Paris , France.
authors.forename: Julien
authors.initials: J
authors.lastname: Claver
authors.affiliation: INSERM UMRS 1149 , Paris , France ; CNRS ERL8252 , Paris , France ; Université Paris Diderot, Sorbonne Paris Cité, Laboratoire d'excellence INFLAMEX , Paris , France.
authors.forename: Neeraj
authors.initials: N
authors.lastname: Tiwari
authors.affiliation: Instituto de Fisiología Celular, Universidad Nacional Autónoma de México , México City , México.
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Sánchez-Miranda
authors.affiliation: Instituto de Fisiología Celular, Universidad Nacional Autónoma de México , México City , México.
authors.forename: Genaro
authors.initials: G
authors.lastname: Vázquez-Victorio
authors.affiliation: Departamento de Farmacobiología, Cinvestav , México City , México.
authors.forename: Karla Alina
authors.initials: KA
authors.lastname: Ramírez-Valadez
authors.affiliation: Instituto de Fisiología Celular, Universidad Nacional Autónoma de México , México City , México.
authors.forename: Marina
authors.initials: M
authors.lastname: Macias-Silva
authors.affiliation: Departamento de Farmacobiología, Cinvestav , México City , México.
authors.forename: Claudia
authors.initials: C
authors.lastname: González-Espinosa
keywords: inflammation; mast cells; secretion; signaling; vesicular trafficking