Journal article
Cutting edge: a novel mechanism for rescue of B cells from CD95/Fas-mediated apoptosis
The Journal of immunology (1950), Vol.163(5), pp.2378-2381
09/01/1999
DOI: 10.4049/jimmunol.163.5.2378
PMID: 10452970
Abstract
CD95-induced apoptosis contributes to the maintenance of homeostasis in both B and T lymphocyte-mediated immunity. B cells increase CD95 expression in response to activation signals and become susceptible to CD95-induced apoptosis. Protection from CD95-mediated death signals can be induced in mature B cells by signals delivered through the B cell Ag receptor. In this paper we demonstrate for the first time that rescue from apoptosis can occur independently of de novo protein synthesis. This rescue from apoptosis prevents activation of caspase 8, the apical caspase in the CD95 death pathway, and CD95-FADD (Fas-associated death domain containing protein) association does not occur normally. Thus B cell activation signals can biochemically modify proximal elements of the CD95 death pathway and regulate the sensitivity of cells to apoptosis induction at an early stage in programmed cell death.
Details
- Title: Subtitle
- Cutting edge: a novel mechanism for rescue of B cells from CD95/Fas-mediated apoptosis
- Creators
- Ian M Catlett - Department of Microbiology, Graduate Program in Immunology, University of Iowa, Veterans Affairs Medical Center, Iowa City 52242, USAGail A Bishop
- Resource Type
- Journal article
- Publication Details
- The Journal of immunology (1950), Vol.163(5), pp.2378-2381
- Publisher
- United States
- DOI
- 10.4049/jimmunol.163.5.2378
- PMID
- 10452970
- ISSN
- 0022-1767
- eISSN
- 1550-6606
- Grant note
- AI28847 / NIAID NIH HHS CA66570 / NCI NIH HHS DK25295 / NIDDK NIH HHS
- Language
- English
- Date published
- 09/01/1999
- Academic Unit
- Microbiology and Immunology; President
- Record Identifier
- 9984002389102771
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