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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Cell+Death+Differ
2016 ; 23
(6
): 1016-25
Nephropedia Template TP
gab.com Text
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English Wikipedia
A blast without power - cell death induced by the tuberculosis-necrotizing toxin
fails to elicit adequate immune responses
#MMPMID26943324
Maueröder C
; Chaurio RA
; Dumych T
; Podolska M
; Lootsik MD
; Culemann S
; Friedrich RP
; Bilyy R
; Alexiou C
; Schett G
; Berens C
; Herrmann M
; Munoz LE
Cell Death Differ
2016[Jun]; 23
(6
): 1016-25
PMID26943324
show ga
In this study, we deploy a doxycycline-dependent suicide switch integrated in a
tumor challenge model. With this experimental setup, we characterized the
immunological consequences of cells dying by four distinct cell death stimuli in
vivo. We observed that apoptotic cell death induced by expression of the
truncated form of BH3 interacting-domain death agonist (tBid) and a
constitutively active form of caspase 3 (revC3), respectively, showed higher
immunogenicity than cell death induced by expression of the
tuberculosis-necrotizing toxin (TNT). Our data indicate that the early release of
ATP induces the silent clearance of dying cells, whereas the simultaneous
presence of 'find me' signals and danger-associated molecular patterns (DAMPs)
promotes inflammatory reactions and increased immunogenicity. This proposed model
is supported by findings showing that the production and release of high
concentrations of IL-27 by bone-marrow-derived macrophages (BMDM) is limited to
BMDM exposed to those forms of death that simultaneously released ATP and the
DAMPs heat-shock protein 90 (HSP90) and high-mobility group box-1 protein
(HMGB1). These results demonstrate that the tissue microenvironment generated by
dying cells may determine the subsequent immune response.
|Alarmins/metabolism
[MESH]
|Animals
[MESH]
|Apoptosis/*drug effects/radiation effects
[MESH]
|BH3 Interacting Domain Death Agonist Protein/genetics/metabolism
[MESH]