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The actin-based motor protein myosin II regulates MHC class II trafficking and BCR-driven antigen presentation

Antigen (Ag) capture and presentation onto major histocompatibility complex (MHC) class II molecules by B lymphocytes is mediated by their surface Ag receptor (B cell receptor [BCR]). Therefore, the transport of vesicles that carry MHC class II and BCR–Ag complexes must be coordinated for them to co...

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Detalles Bibliográficos
Autores principales: Vascotto, Fulvia, Lankar, Danielle, Faure-André, Gabrielle, Vargas, Pablo, Diaz, Jheimmy, Le Roux, Delphine, Yuseff, Maria-Isabel, Sibarita, Jean-Baptiste, Boes, Marianne, Raposo, Graça, Mougneau, Evelyne, Glaichenhaus, Nicolas, Bonnerot, Christian, Manoury, Bénédicte, Lennon-Duménil, Ana-Maria
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064085/
https://www.ncbi.nlm.nih.gov/pubmed/17389233
http://dx.doi.org/10.1083/jcb.200611147
Descripción
Sumario:Antigen (Ag) capture and presentation onto major histocompatibility complex (MHC) class II molecules by B lymphocytes is mediated by their surface Ag receptor (B cell receptor [BCR]). Therefore, the transport of vesicles that carry MHC class II and BCR–Ag complexes must be coordinated for them to converge for processing. In this study, we identify the actin-associated motor protein myosin II as being essential for this process. Myosin II is activated upon BCR engagement and associates with MHC class II–invariant chain complexes. Myosin II inhibition or depletion compromises the convergence and concentration of MHC class II and BCR–Ag complexes into lysosomes devoted to Ag processing. Accordingly, the formation of MHC class II–peptides and subsequent CD4 T cell activation are impaired in cells lacking myosin II activity. Therefore, myosin II emerges as a key motor protein in BCR-driven Ag processing and presentation.