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Yu, X.* ; Ilecka, M.* ; Bartlett, E.J.* ; Schneidt, V.* ; Bhat, R.* ; Mautner, J. ; Feederle, R. ; Delecluse, H.J.*

Antigen-armed antibodies targeting B lymphoma cells effectively activate antigen-specific CD4+ T cells.

Blood 125, 1601-1610 (2015)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The treatment of non-Hodgkin lymphomas has benefited enormously from the introduction of monoclonal antibody-based therapies. However, the efficacy of these treatments varies with lymphoma subtypes and typically decreases with subsequent relapses. Here, we report on antigen-armed antibodies (AgAbs) as a potential treatment for B-cell lymphoma. AgAbs include antigens from ubiquitous pathogens, such as Epstein-Barr virus (EBV), that persist in their host and elicit strong lifelong T cell responses. They act as vectors by introducing antigen directly into tumor cells to induce an antigen-specific CD4+ T cell response against these cells. We have fused antibodies targeting human B-cell surface receptors (CD19-22) to immunodominant T cell antigens from EBV proteins, including EBNA1, EBNA3B and EBNA3C. Exposure of EBV-transformed B-cells and of BL cells to AgAbs led to antigen presentation, T cell recognition and target cell killing. The efficiency of AgAb action paralleled the abundance of the targeted molecules on lymphoma cells as well as their HLA class II expression levels. AgAbs can also induce the activation and proliferation of EBV-specific memory CD4+ T cells ex vivo. These studies show the potential of AgAbs as an effective therapeutic strategy against B-cell lymphomas.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Epstein-barr-virus; Dendritic Cells; Down-regulation; Infection; Responses; Dec-205; Protein; Rituximab; Receptor; Line
ISSN (print) / ISBN 0006-4971
e-ISSN 1528-0020
Zeitschrift Blood
Quellenangaben Band: 125, Heft: 10, Seiten: 1601-1610 Artikelnummer: , Supplement: ,
Verlag American Society of Hematology
Verlagsort Washington
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit Gene Vector (AGV)
Institute of Molecular Immunology (IMI)