Nephrol Dial Transplant (1999) 14: 1831-1834
© 1999 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
The Fas ligand/Fas system in renal injury
Unidad de Diálisis, Fundación Jiménez Díaz, Madrid, Spain
Correspondence and offprint requests to: Alberto Ortiz, Unidad de Diálisis, Fundación Jiménez Díaz, Avda Reyes Católicos 2, 28040 Madrid, Spain.
Introduction
Cell death by apoptosis regulates cell number during induction and resolution of renal injury [1]. Apoptosis inducers include an expanding family of lethal cytokines, that activate a corresponding family of death receptors [2]. The Fas ligand cytokine (FasL/Apo1L/CD95L) and the Fas receptor (Apo1/CD95) belong to these families [2], and evidence is accumulating of their role in renal injury.
FasL and Fas
FasL is a 40-kDa type II transmembrane protein that can be shed in a soluble form by the action of metalloproteinases [2–5]. Soluble FasL is up to 1000-fold less active than membrane-bound FasL in inducing apoptosis [4,5], but promotes neutrophil chemotaxis [6]. Leukocytes, epithelia and tumour cells express FasL [3]. Fas is a 45-kDa type I transmembrane protein that also exists in soluble form [3].
FasL induces apoptosis through Fas cross-linking [
Sources of confusion in the study of the FasL/Fas system
FasL and Fas are expressed in the kidney
Fas induces apoptosis in cultured renal cells
Fas actions in the kidney in vivo
Studies involving loss of function mutations
Summary
Acknowledgments
References
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