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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
DC-NK cell cross talk as a novel CD4⁺ T-cell-independent pathway for antitumor CTL induction.
Blood 106, 338-344 (2005)
It is generally accepted that priming of
antitumor CD8 cytotoxic T lymphocytes
(CTLs) needs help that can be provided
by CD4 T cells. We show that interactions
between dendritic cells (DCs) and
natural killer (NK) cells can bypass the T
helper arm in CTL induction. Bone marrow–
derived DCs caused rejection of the
A20 lymphoma and induced tumor-specific
long-term memory, although they
were not loaded with tumor-derived antigen.
Experiments using CD40 knock-out
mice and cell depletion showed that this
effect did not require CD4 cells. Both
primary rejection and long-term CTL
memory were the result of NK cell activation
by DCs. NK cytotoxicity, which was
necessary for primary rejection, was dependent
on expression of natural killer
group 2 D (NKG2D) ligands on tumor
cells. Blocking of these ligands using
NKG2D tetramers abrogated tumor killing
in vitro and in vivo. The long-term response
was due to CTLs directed against
antigen(s) expressed on A20 and in vitro–
differentiated DCs. The mechanism leading
to CD4 helper cell–independent CTL
responses was elucidated as a cascade
that was initiated by NK cell activation.
This pathway was dependent on interferon-
expression and involved priming
endogenous DCs for interleukin-12 production.
Our data suggest a novel pathway
linking innate and adaptive immunity.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
ISSN (print) / ISBN
0006-4971
e-ISSN
1528-0020
Zeitschrift
Blood
Quellenangaben
Band: 106,
Heft: 1,
Seiten: 338-344
Verlag
American Society of Hematology
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Molecular Immunology (IMI)