Physiological functions of TNF family receptor/ligand interactions in hematopoiesis and transplantation

Secretion of ligands of the tumor necrosis factor (TNF) superfamily is a conserved response of parenchymal tissues to injury and inflammation that commonly perpetuates elimination of dysfunctional cellular components by apoptosis. The same signals of tissue injury that induce apoptosis in somatic ce...

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Bibliographic Details
Published in:Blood 2014-07, Vol.124 (2), p.176-183
Main Authors: Mizrahi, Keren, Askenasy, Nadir
Format: Article
Language:English
Subjects:
Animals
Apoptosis - genetics
Cell Proliferation
Hematopoiesis - physiology
Hematopoietic Stem Cell Transplantation
Hematopoietic Stem Cells - physiology
Humans
Ligands
Multigene Family
Protein Binding
Receptors, Tumor Necrosis Factor - genetics
Receptors, Tumor Necrosis Factor - metabolism
Signal Transduction - genetics
Tumor Necrosis Factor-alpha - metabolism
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Summary:Secretion of ligands of the tumor necrosis factor (TNF) superfamily is a conserved response of parenchymal tissues to injury and inflammation that commonly perpetuates elimination of dysfunctional cellular components by apoptosis. The same signals of tissue injury that induce apoptosis in somatic cells activate stem cells and initiate the process of tissue regeneration as a coupling mechanism of injury and recovery. Hematopoietic stem and progenitor cells upregulate the TNF family receptors under stress conditions and are transduced with trophic signals. The progeny gradually acquires sensitivity to receptor-mediated apoptosis along the differentiation process, which becomes the major mechanism of negative regulation of mature proliferating hematopoietic lineages and immune homeostasis. Receptor/ligand interactions of the TNF family are physiological mechanisms transducing the need for repair, which may be harnessed in pathological conditions and transplantation. Because these interactions are physiological mechanisms of injury, neutralization of these pathways has to be carefully considered in disorders that do not involve intrinsic aberrations of excessive susceptibility to apoptosis.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood-2014-03-559641