Journal ArticleDOI
Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation
Shyr-Te Ju,David J. Panka,Haili Cui,Rachel Ettinger,Maan El-Khatib,David H. Sherr,Ben Z. Stanger,Ann Marshak-Rothstein +7 more
TLDR
It is shown that receptor crosslinking induces Fas ligand and upregulates Fas, and that the ensuing engagement of Fas by Fasligand activates the cell-death programme.Abstract:
Receptor crosslinking of T-cell hybridomas induces cell activation followed by apoptosis. This activation-induced cell death requires de novo synthesis of RNA and proteins, but the actual gene products that provide the death signal have not been identified. We show here that receptor crosslinking induces Fas ligand and upregulates Fas, and that the ensuing engagement of Fas by Fas ligand activates the cell-death programme. Cell death, but not activation, can be selectively prevented by a soluble Fas-immunoglobulin fusion protein. Thus, Fas and Fas ligand are the death-gene products, and their interaction accounts for the molecular mechanism of activation-induced T-cell death.read more
Citations
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The Nuclear Factor NF-κB Pathway in Inflammation
TL;DR: How genetic evidence in mice has revealed complex roles for the NF-kappaB in inflammation that suggest both pro- and anti-inflammatory roles for this pathway is described.
Journal ArticleDOI
Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders.
E. Joanna Baxter,Linda M. Scott,Peter J. Campbell,Clare L. East,Nasios Fourouclas,Soheila Swanton,George S. Vassiliou,Anthony J. Bench,Elaine M. Boyd,Natasha Curtin,Michael A. Scott,Wendy N. Erber,Anthony R. Green,Anthony R. Green +13 more
TL;DR: A single acquired mutation of JAK2 was noted in more than half of patients with a myeloproliferative disorder and its presence in all erythropoietin-independent erythroid colonies demonstrates a link with growth factor hypersensitivity, a key biological feature of these disorders.
Journal ArticleDOI
FADD, a novel death domain-containing protein, interacts with the death domain of fas and initiates apoptosis
TL;DR: Findings suggest that FADD may play an important role in the proximal signal transduction of Fas, a mutant of Fas possessing enhanced killing activity, but not the functionally inactive mutants Fas-LPR and Fas-FD8.
Journal ArticleDOI
Tumoricidal activity of tumor necrosis factor-related apoptosis-inducing ligand in vivo
Henning Walczak,Robert E. Miller,Kiley Ariail,Brian Gliniak,Thomas S. Griffith,Marek Kubin,Wilson Chin,Jon Jones,Anne Woodward,Tiep Le,Craig A. Smith,Pam J. Smolak,Raymond G. Goodwin,Charles Rauch,JoAnn C. L. Schuh,David H. Lynch +15 more
TL;DR: Recurrent treatments with LZ–huTRAIL actively suppressed growth of the TRAIL–sensitive human mammary adenocarcinoma cell line MDA–231 in CB.17 (SCID) mice, and histologic examination of tumors from SCID mice treated with Lz–hu TRAIL demonstrated clear areas of apoptotic necrosis within 9–12 hours of injection.
Journal ArticleDOI
Fas Ligand-Induced Apoptosis as a Mechanism of Immune Privilege
TL;DR: Inflammatory cells entering the anterior chamber of the eye in response to viral infection underwent apoptosis that was dependent on Fas (CD95)-Fas ligand (FasL) and produced no tissue damage.
References
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Journal ArticleDOI
Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction
TL;DR: A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described, providing a pure preparation of undegraded RNA in high yield and can be completed within 4 h.
Journal ArticleDOI
Molecular cloning and expression of the fas ligand, a novel member of the tumor necrosis factor family
TL;DR: Northern hybridization revealed that Fas ligand is expressed in activated splenocytes and thymocytes, consistent with its involvement in T cell-mediated cytotoxicity and in several nonlymphoid tissues, such as testis.
Journal Article
Soluble tumor necrosis factor (TNF) receptors are effective therapeutic agents in lethal endotoxemia and function simultaneously as both TNF carriers and TNF antagonists.
Kendall M. Mohler,Dauphine S. Torrance,Craig A. Smith,Raymond G. Goodwin,K. E. Stremler,V. P. Fung,Hassan Madani,M. B. Widmer +7 more
TL;DR: Results indicate that dimeric sTNFR are effective inhibitors of TNF and under some circumstances function simultaneously as both TNF "carriers" and antagonists of T NF biologic activity.
Journal Article
The cDNA structure, expression, and chromosomal assignment of the mouse Fas antigen.
Rie Watanabe-Fukunaga,Camilynn I. Brannan,Naoto Itoh,Shin Yonehara,Neal G. Copeland,Nancy A. Jenkins,Shigekazu Nagata +6 more
TL;DR: Interspecific backcross analysis indicated that the gene coding for the Fas antigen is in the distal region of mouse chromosome 19, and was significantly induced by treatment with IFN-gamma but not byIFN-alpha/beta.
Journal ArticleDOI
Role for c-myc in activation-induced apoptotic cell death in T cell hybridomas
Yufang Shi,Jacqueline M. Glynn,Lawrence J. Guilbert,Thomas G. Cotter,Reid P. Bissonnette,Douglas R. Green +5 more
TL;DR: Antisense oligonucleotides corresponding to c-myc block the constitutive expression of c-Myc protein in T cell hybridomas and interfere with all aspects of activation-induced apoptosis without affecting lymphokine production in these cells.