PuSH - Publication Server of Helmholtz Zentrum München: Transfer of MHC-class-I molecules among liver sinusoidal cells facilitates hepatic immune surveillance.

Navigation

Home

Deutsch

Research

Advanced Search

Browse by ...

... Journal

... Publication Type

... Research Data

... Publication Year

Publication overview

Support & Contact

Contact persons

Help

Data protection

Schölzel, K.* ; Schildberg, F.A.* ; Welz, M.* ; Borner, C.* ; Geiger, S.* ; Kurts, C.* ; Heikenwälder, M. ; Knolle, P.A.* ; Wohlleber, D.*

Transfer of MHC-class-I molecules among liver sinusoidal cells facilitates hepatic immune surveillance.

J. Hepatol. 61, 600-608 (2014)

DOI

Open Access Green as soon as Postprint is submitted to ZB.

Abstract
Metrics
Extra information

Background & Aims: In the liver, antigen-presenting cell populations such as Kupffer cells, liver dendritic cells, and liver sinusoidal endothelial cells (LSECs) participate through cross-presentation to CD8 T cells (CTLs) in hepatic immune-regulation and immune-surveillance. The participation of hepatic stellate cells (HSCs) in immune regulation is controversial. Here we studied HSC's contribution to antiviral CTL immunity. Methods: Flow cytometric analysis of MHC-I molecules at the cell surface of liver cells from mice with cell-type restricted MHC-I expression. Mice with HSC-restricted MHC-I expression were infected with a hepatotropic virus and analyzed for development of viral hepatitis after CTL transfer. Results: HSCs transferred MHC-I molecules to LSECs and these molecules were employed for LSEC cross-presentation to CTLs. Such transfer of MHC-I molecules was sufficient to support in vivo LSEC cross-presentation of soluble antigens to CTLs. Importantly, this transfer of MHC-I molecules contributed to anti-viral CTL immunity leading to development of immune-mediated hepatitis. Conclusions: Our findings demonstrate transfer of MHC-I molecules among sinusoidal liver cell populations as a potent mechanism to increase anti-viral CTL effector function. The transfer of MHC-I molecules from HSCs supplies LSECs with additional MHC-I molecules for their own cell-intrinsic cross-presentation. Such cross-allocation of MHC-I molecules in liver cell populations is distinct from cross-dressing that occurs among immune cell populations in lymphoid tissues where peptide-loaded MHC-I molecules are transferred. Our findings thus reveal a novel mechanism that increases local cross-presentation and CTL effector function in the liver, which may be instrumental for immune-surveillance during viral infection of antigen-presenting liver cells.

Altmetric

Additional Metrics?

[➜Log in]

Edit extra informations Login

Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Lsec ; Hsc ; Cross-presentation ; Mhc-i; Cross-presentation; Dendritic Cells; T-cells; Stellate Cells; Endothelial-cells; Tolerance Induction; Antigen; Cd8(+); Trogocytosis; Activation

ISSN (print) / ISBN 0168-8278

e-ISSN 1600-0641

Journal Journal of Hepatology

Quellenangaben Volume: 61, Issue: 3, Pages: 600-608

Publisher Elsevier

Publishing Place Amsterdam

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Institute of Virology (VIRO)