Volume 26, Issue 3 pp. 721-724
Short Paper
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Activated B cells express functional Fas ligand

Michael Hahne

Michael Hahne

Institute of Biochemistry, University of Lausanne, Epalinges, Switzerland

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Toufic Renno

Toufic Renno

Ludwig Institute for Cancer Research, University of Lausanne, BIL Research Centre, CH-1066 Epalinges, Switzerland

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Michael Schroeter

Michael Schroeter

Institute of Biochemistry, University of Lausanne, Epalinges, Switzerland

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Martin Irmler

Martin Irmler

Institute of Biochemistry, University of Lausanne, Epalinges, Switzerland

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Lars French

Lars French

Dermatology and Epithelium Network, University of Geneva, Medical School, Geneva, Switzerland

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Thierry Bornand

Thierry Bornand

Institute of Biochemistry, University of Lausanne, Epalinges, Switzerland

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H. Robson MacDonald

H. Robson MacDonald

Ludwig Institute for Cancer Research, University of Lausanne, BIL Research Centre, CH-1066 Epalinges, Switzerland

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Jürg Tschopp

Corresponding Author

Jürg Tschopp

Institute of Biochemistry, University of Lausanne, Epalinges, Switzerland

Institute of Biochemistry, University of Lausanne, Ch. des Boveresses 155, CH-1066 Epalinges, Switzerland (Fax: +41-21-692-5705)Search for more papers by this author
First published: April 1996
Citations: 174

Abstract

Fas ligand (FasL, Apo-1L) is a member of the tumor necrosis factor protein family and binding to its receptor (Fas, Apo-1, CD95) triggers cell death through apoptosis. Ligand expression is restricted to cells with known cytolytic activity and found on hematopoietic cells of the T cell and natural killer lineage. Here we provide evidence that B lymphocytes can express FasL. Flow cytometric analysis revealed that FasL is expressed on the surface of B cells upon stimulation with either lipopolysaccharide or phorbol 12-myristute 13-acetate/ionomycin. FasL expression on activated B cells was confirmed by Western blot and reverse transcriptase polymerase chain reaction analysis. FasL on B cells is functional since lipopolysaccharide-activated B lymphocytes derived from wild type, but not from g/d mutant mice, were able to kill Fas-sensitive target cells. Our data suggest that the Fas system may contribute to the control of B cell homeostasis.

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