(Q57384656)

English

Resistance of cultured peripheral T cells towards activation-induced cell death involves a lack of recruitment of FLICE (MACH/caspase 8) to the CD95 death-inducing signaling complex

scholarly article by Marcus E. Peter et al published May 1997 in European Journal of Immunology

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scholarly article

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Resistance of cultured peripheral T cells towards activation-induced cell death involves a lack of recruitment of FLICE (MACH/caspase 8) to the CD95 death-inducing signaling complex (English)

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Klaus-Michael Debatin

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Klaus-Michael Debatin

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author name string

Marcus E. Peter

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Frank C. Kischkel

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Christian G. Scheuerpflug

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Jan Paul Medema

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Peter H. Krammer

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language of work or name

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publication date

May 1997

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European Journal of Immunology

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27

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1207-1212

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5

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The role of APO-1-mediated apoptosis in the immune system

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Activation interferes with the APO-1 pathway in mature human T cells.

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Interleukin-2 programs mouse alpha beta T lymphocytes for apoptosis

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DNA fragmentation and cell death is selectively triggered in activated human lymphocytes by Fas antigen engagement

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Autocrine T-cell suicide mediated by APO-1/(Fas/CD95)

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Fas ligand mediates activation-induced cell death in human T lymphocytes

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Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas.

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Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation.

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The fas antigen is involved in peripheral but not thymic deletion of T lymphocytes in T cell receptor transgenic mice

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FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis

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A novel protein that interacts with the death domain of Fas/APO1 contains a sequence motif related to the death domain

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FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex

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Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death

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Human ICE/CED-3 protease nomenclature

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Monoclonal antibody-mediated tumor regression by induction of apoptosis.

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RIP: a novel protein containing a death domain that interacts with Fas/APO-1 (CD95) in yeast and causes cell death

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Defective expression of hematopoietic cell protein tyrosine phosphatase (HCP) in lymphoid cells blocks Fas-mediated apoptosis

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FAP-1: a protein tyrosine phosphatase that associates with Fas

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CD28 costimulation can promote T cell survival by enhancing the expression of Bcl-XL.

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The role of bcl-XL in CD40-mediated rescue from anti-mu-induced apoptosis in WEHI-231 B lymphoma cells

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The roles of costimulation and Fas in T cell apoptosis and peripheral tolerance

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Induction of apoptosis in mature T cells by tumour necrosis factor

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The roles of Fas/APO-1 (CD95) and TNF in antigen-induced programmed cell death in T cell receptor transgenic mice.

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Homeostatic regulation of CD8+ T cells after antigen challenge in the absence of Fas (CD95)

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Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection

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Apoptosis, Fas and systemic autoimmunity: the MRL-lpr/lpr model

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Identifiers

10.1002/EJI.1830270523

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