Autophagy promotes MHC class II presentation of peptides from intracellular source proteins

Publikation

Autophagy promotes MHC class II presentation of peptides from intracellular source proteins

Wissenschaftlicher Artikel/Review - 31.05.2005

Dengjel Jörn, Rammensee Hans-Georg, Driessen Christoph, Brock Roland, Kalbacher Hubert, Brandenburg Jens, Altenberend Florian, Kreymborg Katharina, Müller Margret, Kraus Marianne, Reich Michael, Fischer Rainer, Schoor Oliver, Stevanovic Stefan

Zitation

Dengjel J, Rammensee H, Driessen C, Brock R, Kalbacher H, Brandenburg J, Altenberend F, Kreymborg K, Müller M, Kraus M, Reich M, Fischer R, Schoor O, Stevanovic S. Autophagy promotes MHC class II presentation of peptides from intracellular source proteins. Proceedings of the National Academy of Sciences of the United States of America 2005; 102:7922-7.

Art

Wissenschaftlicher Artikel/Review (Englisch)

Zeitschrift

Proceedings of the National Academy of Sciences of the United States of America 2005; 102

Veröffentlichungsdatum

31.05.2005

ISSN (Druck)

0027-8424

Seiten

7922-7

Kurzbeschreibung/Zielsetzung

MHC-peptide complexes mediate key functions in adaptive immunity. In a classical view, MHC-I molecules present peptides from intracellular source proteins, whereas MHC-II molecules present antigenic peptides from exogenous and membrane proteins. Nevertheless, substantial crosstalk between these two pathways has been observed. We investigated the influence of autophagy on the MHC-II ligandome and demonstrated that peptide presentation is altered considerably upon induction of autophagy. The presentation of peptides from intracellular and lysosomal source proteins was strongly increased on MHC-II in contrast with peptides from membrane and secreted proteins. In addition, autophagy influenced the MHC-II antigen-processing machinery. Our study illustrates a profound influence of autophagy on the class II peptide repertoire and suggests that this finding has implications for the regulation of CD4(+) T cell-mediated processes.