Antigen processing and presentation by dendritic cells is independent of coronin 1
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 1434416
Author(s) Westritschnig, Katrin; BoseDasgupta, Somdeb; Tchang, Vincent; Siegmund, Kerstin; Pieters, Jean
Author(s) at UniBasel Pieters, Jean
Year 2012
Title Antigen processing and presentation by dendritic cells is independent of coronin 1
Journal Molecular immunology
Volume 53
Number 4
Pages / Article-Number 379-86
Keywords Coronin 1, Dendritic cells, Antigen processing and presentation, T cell stimulation
Abstract

Coronin 1, which is a member of the evolutionary conserved coronin protein family that is highly expressed in all leukocytes is involved in the activation of the Ca(2+)/calcineurin signaling pathway following cell surface stimulation in T cells, B cells as well as macrophages. Mice deficient for coronin 1 have strongly reduced peripheral T cell numbers as a result of a lack of pro-survival signals for naïve T cells. Whether or not impaired antigen processing and presentation in the absence of coronin 1 expression contributes to this reduction of T cell numbers is unknown. We here show that coronin 1-deficient bone marrow-derived dendritic cells develop normally, and that wild type and coronin 1-deficient dendritic cells were equally able to induce antigen-specific proliferation of T cells. Furthermore, upon immunization, in vivo proliferation of adoptively transferred antigen-specific T cells was comparable in wild type and coronin 1-deficient mice. Finally, infection of wild type and coronin 1-deficient dendritic cells with an ovalbumin-expressing Listeria monocytogenes strain induced comparable levels of ovalbumin-specific T cells responses. Together these results suggest that coronin 1 is dispensable for antigen processing and presentation by dendritic cells.

Publisher Pergamon Press
ISSN/ISBN 0161-5890
edoc-URL http://edoc.unibas.ch/dok/A6043795
Full Text on edoc No
Digital Object Identifier DOI 10.1016/j.molimm.2012.09.002
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/23099476
ISI-Number WOS:000314377800009
Document type (ISI) Journal Article
 
   

MCSS v5.8 PRO. 0.448 sec, queries - 0.000 sec ©Universität Basel  |  Impressum   |    
08/08/2020