Activated Human T Cells Release Bioactive Fas Ligand and APO2 Ligand in Microvesicles-Reference-Cited by-同舟云学术

Activated Human T Cells Release Bioactive Fas Ligand and APO2 Ligand in Microvesicles

Published:1999-08-01 Issue:3 Volume:163 Page:1274-1281
ISSN:0022-1767
Container-title:The Journal of Immunology
language:en
Short-container-title:

Author:

Martínez-Lorenzo María José¹,Anel Alberto¹,Gamen Susana¹,Monleón Inmaculada¹,Lasierra Pilar²,Larrad Luis²,Piñeiro Andrés¹,Alava María A.¹,Naval Javier¹

Affiliation:

1. *Departamento de Bioquímica y Biología Molecular y Cellular, Facultad de Ciencias, and

2. †Servicio de Inmunología, Hospital Clínico Universitario, Universidad de Zaragoza, Zaragoza, Spain

Abstract

Abstract Activation-induced cell death is a process by which overactivated T cells are eliminated, thus preventing potential autoimmune attacks. Two known mediators of activation-induced cell death are Fas(CD95) ligand (FasL) and APO2 ligand (APO2L)/TNF-related apoptosis-inducing ligand (TRAIL). We show here that upon mitogenic stimulation, bioactive FasL and APO2L are released from the T cell leukemia Jurkat and from normal human T cell blasts as intact, nonproteolyzed proteins associated with a particulate, ultracentrifugable fraction. We have characterized this fraction as microvesicles of 100–200 nm in diameter. These microvesicles are released from Jurkat and T cell blasts shortly (≤1 h) after PHA stimulation, well before the cell enters apoptosis. FasL- and APO2L-containing vesicles are also present in supernatants from PHA-activated fresh human PBMC. These observations provide the basis for a new and efficient mechanism for the rapid induction of autocrine or paracrine cell death during immune regulation.

Publisher

The American Association of Immunologists

Subject

Immunology,Immunology and Allergy

Link

https://journals.aai.org/jimmunol/article-pdf/163/3/1274/1107353/im159901274p.pdf

Reference47 articles.

1. Russell, J. H.. 1995. Activation-induced death of mature T cells in the regulation of immune responses. Curr. Opin. Immunol. 7: 382

2. Dhein, J., H. Walczak, C. Bäumler, K. M. Debatin, P. H. Krammer. 1995. Autocrine T-cell suicide mediated by APO-1 (Fas/CD95). Nature 373: 438

3. Brunner, T., R. J. Mogil, D. LaFace, N. J. Yoo, A. Mahboubi, F. Echeverri, S. J. Martin, W. R. Force, D. H. Lynch, C. F. Ware, et al 1995. Cell-autonomous Fas(CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas. Nature 373: 441

4. Ju, S. T., D. J. Panka, H. Cui, R. Ettinger, M. El-Khatib, D. H. Sherr, B. Z. Stanger, A. Marshak-Rothstein. 1995. Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation. Nature 373: 444

5. Vignaux, F., P. Golstein. 1994. Fas-based lymphocyte-mediated cytotoxicity against syngeneic activated lymphocytes: a regulatory pathway?. Eur. J. Immunol. 24: 923

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