Inhibition of glucocorticoid-mediated, caspase-independent dendritic cell death by CD40 activation
- Authors
- Kim, KD; Choe, YK; Choe, IS; Lim, JS
- Issue Date
- Mar-2001
- Publisher
- FEDERATION AMER SOC EXP BIOL
- Keywords
- CD40 signaling; dexamethasone; apoptosis
- Citation
- JOURNAL OF LEUKOCYTE BIOLOGY, v.69, no.3, pp 426 - 434
- Pages
- 9
- Journal Title
- JOURNAL OF LEUKOCYTE BIOLOGY
- Volume
- 69
- Number
- 3
- Start Page
- 426
- End Page
- 434
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/149692
- DOI
- 10.1189/jlb.69.3.426
- ISSN
- 0741-5400
1938-3673
- Abstract
- Glucocorticoids (GC) are potent antiinflammatory and immunosuppressive agents that act on a variety of immune cells, including T cells, monocytes/macrophages, osteoclasts, and dendritic cells (DC), However, the mechanism(s) by which GC exert anti-inflammatory effects is still largely unknown. It is already well known that GC treatment inhibits DC maturation and interleukin (IL)-12 production by DC. In this study, we investigated the apoptosis induction of DC by a synthetic GC, dexamethasone (Dex), The stimulation with Dex resulted in DC apoptosis in a dose- and time-dependent manner as it was measured by determining annexin V-positive cells and mitochondrial potential. In contrast, monocytes that are precursor cells of DC are resistant to Dex-mediated apoptosis. The Dex-induced apoptosis of DC was independent of caspase activation because it was not inhibited by the broad caspase inhibitor, Z-VAD-fmk, It is interesting that agonistic CD40 antibody completely inhibited Dex-induced cell death, whereas other inflammatory stimuli did not show the same effect, suggesting that CD40 signaling may selectively modulate CC-mediated DC apoptosis, Taken together, our findings revealed an important role of GC: and CD40 signaling in the regulation of immune responses in which DC play a key role in the inflammatory process of
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - 이과대학 > 생명시스템학부 > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.