Document Detail

Induction of exosome release in primary B cells stimulated via CD40 and the IL-4 receptor.
MedLine Citation:
PMID:  18523279     Owner:  NLM     Status:  MEDLINE    
Exosomes are lipid-bound nanovesicles formed by inward budding of the endosomal membrane and released following fusion of the endosomal limiting membrane with the plasma membrane. We show here that primary leukocytes do not release exosomes unless subjected to potent activation signals, such as cytokine or mitogen stimulation. In particular, high levels of exosomes were released when murine splenic B cells were stimulated via CD40 and the IL-4 receptor. This property was shared by B cells from different anatomic locations, as newly formed marginal zone and follicular B cells were capable of secreting exosomes upon CD40/IL-4 triggering. B cell exosomes expressed high levels of MHC class I, MHC class II, and CD45RA (B220), as well as components of the BCR complex, namely, surface Ig, CD19, and the tetraspanins CD9 and CD81. Ig on the plasma membrane of primary B cells was targeted to the exosome pathway, demonstrating a link between the BCR and this exocytic pathway. IgD and IgM were the predominant Ig isotypes associated with CD40/IL-4 elicited exosomes, though other isotypes (IgA, IgG1, IgG2a/2b, and IgG3) were also detected. Together, these results suggest that exosome release is not constitutive activity of B cells, but may be induced following cell: cell signaling.
Sarah C Saunderson; Petra C Schuberth; Amy C Dunn; Lilija Miller; Barry D Hock; Philippa A MacKay; Norbert Koch; Ralph W Jack; Alexander D McLellan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  180     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-06-04     Completed Date:  2008-09-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  8146-52     Citation Subset:  AIM; IM    
Department of Microbiology and Immunology, Christchurch School of Medicine, University of Otago, Dunedin, New Zealand.
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MeSH Terms
Antigen-Presenting Cells / immunology,  secretion
Antigens, CD40 / physiology*
B-Lymphocyte Subsets / immunology*,  secretion*
Cell Line, Tumor
Cells, Cultured
Cytoplasmic Vesicles / immunology*,  secretion*
Exocytosis / immunology*
Histocompatibility Antigens Class I / metabolism
Histocompatibility Antigens Class II / metabolism
Lymphocyte Activation / immunology*
Mice, Inbred BALB C
Receptors, Interleukin-4 / physiology*
Spleen / cytology,  immunology,  secretion
Reg. No./Substance:
0/Antigens, CD40; 0/Histocompatibility Antigens Class I; 0/Histocompatibility Antigens Class II; 0/Receptors, Interleukin-4

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