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Ortner, D.* ; Grabher, D.* ; Hermann, M.* ; Kremmer, E. ; Hofer, S.* ; Heufler, C.*

The adaptor protein Bam32 in human dendritic cells participates in the regulation of MHC class I-induced CD8+ T cell activation.

J. Immunol. 187, 3972-3978 (2011)
Verlagsversion Forschungsdaten DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The B lymphocyte adaptor molecule of 32 kDa (Bam32) is strongly induced during the maturation of dendritic cells (DC). Most known functions of Bam32 are related to the signaling of the B cell receptor for Ag. Because DC do not express receptors specific for Ags, we aim at characterizing the role of Bam32 in human monocyte-derived DC in this study. Our results show that binding of allogeneic T cells to mature DC causes accumulation of Bam32 on the contact sites and that this translocation is mimicked by Ab-mediated engagement of MHC class I. Silencing of Bam32 in mature monocyte-derived DC results in an enhanced proliferation of CD8(+) T cells in an Ag-specific T cell proliferation assay. Further studies identify galectin-1 as an intracellular binding partner of Bam32. Regulating immune responses via regulatory T cell (Treg) modulation is one of the many immunological activities attributed to galectin-1. Therefore, we assayed mixed leukocyte reactions for Treg expansion and found fewer Treg in reactions stimulated with DC silenced for Bam32 compared to reactions stimulated with DC treated with a nontarget control. Based on our findings, we propose a role for Bam32 in the signaling of MHC class I molecules in professional Ag-presenting DC for the regulation of CD8(+) T cell activation. It is distinct from that of MHC class I recognized by CD8(+) T cells leading to T cell death. Thus, our data pinpoint a novel level of T cell regulation that may be of biological relevance.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Epidermal langerhans cells; Phosphatidylinositol 3-Kinase; Galectin-1; Blood; Lymphocytes; BAM32/DAPP1; Maturation; Generation; Molecule; Effector
Sprache englisch
Veröffentlichungsjahr 2011
HGF-Berichtsjahr 2011
ISSN (print) / ISBN 0022-1767
e-ISSN 1550-6606
Zeitschrift Journal of Immunology
Quellenangaben Band: 187, Heft: 8, Seiten: 3972-3978 Artikelnummer: , Supplement: ,
Verlag American Association of Immunologists
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)
PSP-Element(e) G-501700-003
PubMed ID 21930970
DOI 10.4049/jimmunol.1003072
Scopus ID 80054762002
Erfassungsdatum 2011-11-24
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