The human melanoma cell line MelJuSo secretes bioactive FasL and APO2L/TRAIL on the surface of microvesicles. Possible contribution to tumor counterattack (Q40565480)

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scientific article published on May 2004

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English	The human melanoma cell line MelJuSo secretes bioactive FasL and APO2L/TRAIL on the surface of microvesicles. Possible contribution to tumor counterattack	scientific article published on May 2004

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scholarly article

1 reference

Europe PubMed Central

21 September 2017

The human melanoma cell line MelJuSo secretes bioactive FasL and APO2L/TRAIL on the surface of microvesicles. Possible contribution to tumor counterattack (English)

1 reference

Europe PubMed Central

21 September 2017

author name string

María José Martínez-Lorenzo

1

1 reference

Europe PubMed Central

21 September 2017

Alberto Anel

2

1 reference

Europe PubMed Central

21 September 2017

María A Alava

3

1 reference

Europe PubMed Central

21 September 2017

Andrés Piñeiro

4

1 reference

Europe PubMed Central

21 September 2017

Javier Naval

5

1 reference

Europe PubMed Central

21 September 2017

Pilar Lasierra

6

1 reference

Europe PubMed Central

21 September 2017

Luis Larrad

7

1 reference

Europe PubMed Central

21 September 2017

language of work or name

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publication date

1 May 2004

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Europe PubMed Central

21 September 2017

Experimental Cell Research

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Europe PubMed Central

21 September 2017

295

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Europe PubMed Central

21 September 2017

2

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Europe PubMed Central

21 September 2017

315-329

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Europe PubMed Central

21 September 2017

The Fas death factor

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Cytotoxic T lymphocytes: all roads lead to death

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Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity

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Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient mice

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Decreased tumor surveillance in perforin-deficient mice

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Fas and Fas ligand interactions suppress melanoma lung metastasis

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Tumor immunity in perforin-deficient mice: a role for CD95 (Fas/APO-1)

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A central role for death receptor-mediated apoptosis in the rejection of tumors by NK cells

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Tumor-specific CTL kill murine renal cancer cells using both perforin and Fas ligand-mediated lysis in vitro, but cause tumor regression in vivo in the absence of perforin

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Induction of apoptosis by Apo-2 ligand, a new member of the tumor necrosis factor cytokine family

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Melanoma cell expression of Fas(Apo-1/CD95) ligand: implications for tumor immune escape

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Functional Consequences of APO-1/Fas (CD95) Antigen Expression by Normal and Neoplastic Hematopoietic Cells

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The Fas counterattack: Fas-mediated T cell killing by colon cancer cells expressing Fas ligand

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Expression of CD95 ligand in melanocytic lesions as a diagnostic marker

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Cutting Edge: The Tumor Counterattack Hypothesis Revisited: Colon Cancer Cells Do Not Induce T Cell Apoptosis Via the Fas (CD95, APO-1) Pathway

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Not so Fas: Re-evaluating the mechanisms of immune privilege and tumor escape

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Regulation of cell surface APO-1/Fas (CD95) ligand expression by metalloproteases

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Expression of the functional soluble form of human fas ligand in activated lymphocytes.

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Conversion of membrane-bound Fas(CD95) ligand to its soluble form is associated with downregulation of its proapoptotic activity and loss of liver toxicity

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Membrane Fas ligand kills human peripheral blood T lymphocytes, and soluble Fas ligand blocks the killing

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Downregulation of Fas ligand by shedding

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Differential secretion of Fas ligand- or APO2 ligand/TNF-related apoptosis-inducing ligand-carrying microvesicles during activation-induced death of human T cells

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Influence of alpha-melanocyte-stimulating hormone and ultraviolet radiation on the transfer of melanosomes to keratinocytes

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Involvement of APO2 ligand/TRAIL in activation-induced death of Jurkat and human peripheral blood T cells

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Doxorubicin treatment activates a Z-VAD-sensitive caspase, which causes deltapsim loss, caspase-9 activity, and apoptosis in Jurkat cells

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Mast cell-dependent B and T lymphocyte activation is mediated by the secretion of immunologically active exosomes

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Release of preformed Fas ligand in soluble form is the major factor for activation-induced death of Jurkat T cells

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Reduction in mitochondrial potential constitutes an early irreversible step of programmed lymphocyte death in vivo.

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Direct vesicular transport of MHC class II molecules from lysosomal structures to the cell surface

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B lymphocytes secrete antigen-presenting vesicles

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Selective enrichment of tetraspan proteins on the internal vesicles of multivesicular endosomes and on exosomes secreted by human B-lymphocytes.

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Signal transduction. FasL binds preassembled Fas

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Induction of lymphocyte apoptosis by tumor cell secretion of FasL-bearing microvesicles.

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Tumor-derived exosomes are a source of shared tumor rejection antigens for CTL cross-priming

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The membrane-bound but not the soluble form of human Fas ligand is responsible for its inflammatory activity

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Fas ligand breaks tolerance to self-antigens and induces tumor immunity mediated by antibodies

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Fas ligand engagement of resident peritoneal macrophages in vivo induces apoptosis and the production of neutrophil chemotactic factors

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Regulation of the proinflammatory effects of Fas ligand (CD95L).

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Is cancer dangerous to the immune system?

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10.1016/J.YEXCR.2003.12.024

1 reference

Europe PubMed Central

21 September 2017

1 reference

Europe PubMed Central

21 September 2017

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