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SLE serum induces classical caspase-dependent apoptosis independent of death receptors

Bengtsson, Anders LU ; Gullstrand, Birgitta LU ; Truedsson, Lennart LU and Sturfelt, Gunnar LU (2008) In Clinical Immunology 126(1). p.57-66
Abstract
The main source of autoantigens in systemic lupus erythematosus (SLE) is most likely apoptotic material. We have previously shown that sera from SLE patients can induce apoptosis in monocytes and lymphocytes, and here we characterized mechanisms of apoptosis induced by SLE serum. SLE serum seems to induce caspase-dependent classical apoptosis since cells exposed to SLE serum displayed morphology consistent with classical apoptosis as demonstrated by confocal microscopy, and pan-caspase inhibitor Z-VAD.fmk significantly reduced SLE serum-induced apoptosis. Death-receptor-independent pathways seemed to be involved since SLE serum induced apoptosis equally in FADD-mutant and wild-type Jurkat cell lines, and blocking of Fas and TNFR1 did not... (More)
The main source of autoantigens in systemic lupus erythematosus (SLE) is most likely apoptotic material. We have previously shown that sera from SLE patients can induce apoptosis in monocytes and lymphocytes, and here we characterized mechanisms of apoptosis induced by SLE serum. SLE serum seems to induce caspase-dependent classical apoptosis since cells exposed to SLE serum displayed morphology consistent with classical apoptosis as demonstrated by confocal microscopy, and pan-caspase inhibitor Z-VAD.fmk significantly reduced SLE serum-induced apoptosis. Death-receptor-independent pathways seemed to be involved since SLE serum induced apoptosis equally in FADD-mutant and wild-type Jurkat cell lines, and blocking of Fas and TNFR1 did not reduce apoptosis induction. Importantly, apoptosis was significantly reduced in a Bcl-2 overexpressing Jurkat cell line indicating involvement of mitochondrial pathways. Thus, based on morphology and caspase inhibition experiments, we have demonstrated that SLE serum induce classical caspase-dependent apoptosis, and this was independent of death receptor pathways. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Clinical Immunology
volume
126
issue
1
pages
57 - 66
publisher
Elsevier
external identifiers
  • pmid:18036993
  • wos:000252416400006
  • scopus:37249009222
ISSN
1521-6616
DOI
10.1016/j.clim.2007.10.003
language
English
LU publication?
yes
id
3356cb16-7680-4c8f-9eee-079d16a5aa38 (old id 1140044)
date added to LUP
2008-07-28 14:31:00
date last changed
2017-04-16 03:35:48
@article{3356cb16-7680-4c8f-9eee-079d16a5aa38,
  abstract     = {The main source of autoantigens in systemic lupus erythematosus (SLE) is most likely apoptotic material. We have previously shown that sera from SLE patients can induce apoptosis in monocytes and lymphocytes, and here we characterized mechanisms of apoptosis induced by SLE serum. SLE serum seems to induce caspase-dependent classical apoptosis since cells exposed to SLE serum displayed morphology consistent with classical apoptosis as demonstrated by confocal microscopy, and pan-caspase inhibitor Z-VAD.fmk significantly reduced SLE serum-induced apoptosis. Death-receptor-independent pathways seemed to be involved since SLE serum induced apoptosis equally in FADD-mutant and wild-type Jurkat cell lines, and blocking of Fas and TNFR1 did not reduce apoptosis induction. Importantly, apoptosis was significantly reduced in a Bcl-2 overexpressing Jurkat cell line indicating involvement of mitochondrial pathways. Thus, based on morphology and caspase inhibition experiments, we have demonstrated that SLE serum induce classical caspase-dependent apoptosis, and this was independent of death receptor pathways.},
  author       = {Bengtsson, Anders and Gullstrand, Birgitta and Truedsson, Lennart and Sturfelt, Gunnar},
  issn         = {1521-6616},
  language     = {eng},
  number       = {1},
  pages        = {57--66},
  publisher    = {Elsevier},
  series       = {Clinical Immunology},
  title        = {SLE serum induces classical caspase-dependent apoptosis independent of death receptors},
  url          = {http://dx.doi.org/10.1016/j.clim.2007.10.003},
  volume       = {126},
  year         = {2008},
}