Abstract
OPINION article Front. Immunol., 27 March 2017Sec. Immunological Tolerance and Regulation Volume 8 - 2017 | https://doi.org/10.3389/fimmu.2017.00342
Highlights
Receptor/ligand interactions of the tumor necrosis factor (TNF) superfamily are associated with versatile apoptotic and regulatory signaling pathways in parenchymal tissues and the immunohematopoietic system
Apoptotic signaling mediated by Fas and TNF receptor-1 (TNF-R1) is one of the major cytotoxic mechanisms used by immune cells to kill endogenous cells and exogenous pathogens
These ubiquitous effector mechanisms of cell death, along with perforin/granzyme, are direct mediators of β-cell injury that is inflicted in autoimmune insulitis in type 1 diabetes (T1D)
Summary
Receptor/ligand interactions of the tumor necrosis factor (TNF) superfamily are associated with versatile apoptotic and regulatory signaling pathways in parenchymal tissues and the immunohematopoietic system. The Fas/FasL interaction is a common effector mechanism of β-cell apoptosis and islet injury under inflammatory conditions, and physiological modulation of immune homeostasis, including control of aberrant autoimmune reactions. The physiological significance of this receptor/ligand interaction is emphasized by lymphoproliferative disorders resulting from disruption of homeostatic negative regulation in Fas-deficient (lpr) and FasL-defective (gld) mice [13] Despite these particular characteristics of the Fas/FasL interaction, common physiological trophic and apoptotic activities are shared by soluble ligands of the TNF superfamily, including TNFα and TNF-related apoptosis-inducing ligand receptor-1 [8]. The Fas signaling pathway is involved in regulation of insulin secretion [14, 15]
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