PuSH - Publication Server of Helmholtz Zentrum München

Stern, J.N.* ; Keskin, D.B.* ; Kato, Z.* ; Waldner, H.* ; Schallenberg, S.* ; Anderson, A.C.* ; von Boehmer, H.* ; Kretschmer, K.* ; Strominger, J.L.*

Promoting tolerance to proteolipid protein-induced experimental autoimmune encephalomyelitis through targeting dendritic cells.

Proc. Natl. Acad. Sci. U.S.A. 107, 17280-17285 (2010)
DOI PMC
Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
In T cell-mediated autoimmune diseases, self-reactive T cells with known antigen specificity appear to be particularly promising targets for antigen-specific induction of tolerance without compromising desired protective host immune responses. Several lines of evidence suggest that delivery of antigens to antigen-presenting dendritic cells (DCs) in the steady state (i.e., to immature DCs) may represent a suitable approach to induce antigen-specific T-cell tolerance peripherally. Here, we report that anti-DEC205-mediated delivery of the self-peptide proteolipid protein (PLP)139-151 to DCs ameliorated clinical symptoms in the PLP-induced SJL model of experimental autoimmune encephalomyelitis. Splenocytes from treated mice were anergized to PLP139-151, and IL-17 secretion was markedly reduced. Moreover, we show directly, using transgenic CD4(+) Vβ6(+) TCR T cells specific for PLP139-151, that, under the conditions of the present experiments, these cells also became anergic. In addition, evidence for a CD4(+) T cell-mediated suppressor mechanism was obtained.
Impact Factor
Scopus SNIP
Scopus
Cited By
Altmetric
0.000
3.610
54
Tags
Annotations
Special Publikation
Hide on homepage

Edit extra information
Edit own tags
Private
Edit own annotation
Private
Hide on publication lists
on hompage
Mark as special
publikation
Publication type Article: Journal article
Document type Scientific Article
Language english
Publication Year 2010
HGF-reported in Year 0
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Quellenangaben Volume: 107, Issue: 40, Pages: 17280-17285 Article Number: , Supplement: ,
Publisher National Academy of Sciences
Reviewing status Peer reviewed
Institute(s) Institute of Pancreatic Islet Research (IPI)
PubMed ID 20855626
Erfassungsdatum 2010-12-31