
DOI . ORG {
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Title[redir]:
Myeloid-derived suppressor cells (MDSC): an important partner in cellular/tissue senescence | Biogerontology
Description:
The aging process is associated with a low-grade chronic inflammation and the accumulation of senescent cells into tissues. Diverse stresses can trigger cellular senescence, a cell fate characterized by cell-cycle arrest and flat morphology. Oncogenic signaling can also induce cellular senescence which has been termed oncogene-induced senescence (OIS). Senescent cells display a pro-inflammatory phenotype which has been called the senescence-associated secretory phenotype (SASP). The secretomes associated with SASP contain colony-stimulating factors and chemokines which stimulate the generation of myeloid-derived suppressor cells (MDSC) by enhancing myelopoiesis in bone marrow and spleen. Enhanced myelopoiesis and increased level of MDSCs have been observed in bone marrow, spleen, and blood in both tumor-bearing and aged mice. Immunosuppressive MDSCs are recruited via chemotaxis into inflamed tissues where they proliferate and consequently suppress acute inflammatory reactions by inhibiting the functions of distinct components of innate and adaptive immunity. For instance, MDSCs stimulate the activity of immunosuppressive regulatory T-cells (Tregs). They also increase the expression of amino acid catabolizing enzymes and the secretion of anti-inflammatory cytokines, e.g. IL-10 and TGF-β, and reactive oxygen species (ROS). On the other hand, the accumulation of MDSCs into tissues exerts harmful effects in chronic pathological disorders, e.g. tumors and many age-related diseases, since the immunosuppression induced by MDSCs impairs the clearance of senescent and cancer cells and also disturbs the maintenance of energy metabolism and tissue proteostasis. The co-operation between senescent cells and immunosuppressive MDSCs regulates not only tumorigenesis and chronic inflammatory disorders but it also might promote inflammaging during the aging process.
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Keywords {🔍}
pubmed, article, google, scholar, cas, cells, central, suppressor, myeloidderived, cell, senescence, cancer, aging, immunol, cellular, senescent, tumor, biol, myeloid, ageing, wang, res, rev, campisi, inflammation, mdscs, human, role, liu, inflammatory, nat, immune, regulatory, phenotype, secretory, macrophages, van, zhang, bone, marrow, mice, stem, disease, trends, chen, yang, finland, function, accumulation, signaling,
Topics {✒️}
hematopoietic stem cells cxcl2/mif-cxcr2 signaling promotes muscle-derived nitric oxide myeloid-derived suppressor cells month download article/chapter cell surface-bound il-1α human dendritic cells decreased tnf-α synthesis cell-mediated liver injury myeloid-derived cells myeloid suppressor cells immunosuppressive regulatory t-cells immature myeloid cells molecular structure-functional activity /ebpβ enhances nf-κb pge2-induced cxcl12 production termed oncogene-induced senescence oncogene-induced senescence relayed interleukin-dependent inflammatory network low-grade chronic inflammation nf-κb-dependent mechanism /ebpβ transcription factor de keizer plj article biogerontology aims full article pdf dendritic cells il-6/il-8 cytokine network pleiotropic-inflamed monocytes/macrophages age-related degenerative disease davalos ar promote macrophage migration induce cellular senescence reactive oxygen species alternately activated macrophages induces cellular senescence morales-rosales sl retinoblastoma tumor suppressor van deursen jm privacy choices/manage cookies dna damage response immune-suppressive cells article salminen childs bg burton dg limits tumor progression van de sluis senescent cells display targeting senescent cells p53 tumor suppressor impair antitumor immunity
Questions {❓}
- Campisi J, Andersen JK, Kapahi P, Melov S (2011) Cellular senescence: a link between cancer and age-related degenerative disease?
- Goh C, Narayanan S, Hahn YS (2013) Myeloid-derived suppressor cells: the dark knight or the joker in viral infections?
- De Keizer PL (2017) The fountain of youth by targeting senescent cells?
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headline:Myeloid-derived suppressor cells (MDSC): an important partner in cellular/tissue senescence
description:The aging process is associated with a low-grade chronic inflammation and the accumulation of senescent cells into tissues. Diverse stresses can trigger cellular senescence, a cell fate characterized by cell-cycle arrest and flat morphology. Oncogenic signaling can also induce cellular senescence which has been termed oncogene-induced senescence (OIS). Senescent cells display a pro-inflammatory phenotype which has been called the senescence-associated secretory phenotype (SASP). The secretomes associated with SASP contain colony-stimulating factors and chemokines which stimulate the generation of myeloid-derived suppressor cells (MDSC) by enhancing myelopoiesis in bone marrow and spleen. Enhanced myelopoiesis and increased level of MDSCs have been observed in bone marrow, spleen, and blood in both tumor-bearing and aged mice. Immunosuppressive MDSCs are recruited via chemotaxis into inflamed tissues where they proliferate and consequently suppress acute inflammatory reactions by inhibiting the functions of distinct components of innate and adaptive immunity. For instance, MDSCs stimulate the activity of immunosuppressive regulatory T-cells (Tregs). They also increase the expression of amino acid catabolizing enzymes and the secretion of anti-inflammatory cytokines, e.g. IL-10 and TGF-β, and reactive oxygen species (ROS). On the other hand, the accumulation of MDSCs into tissues exerts harmful effects in chronic pathological disorders, e.g. tumors and many age-related diseases, since the immunosuppression induced by MDSCs impairs the clearance of senescent and cancer cells and also disturbs the maintenance of energy metabolism and tissue proteostasis. The co-operation between senescent cells and immunosuppressive MDSCs regulates not only tumorigenesis and chronic inflammatory disorders but it also might promote inflammaging during the aging process.
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description:The aging process is associated with a low-grade chronic inflammation and the accumulation of senescent cells into tissues. Diverse stresses can trigger cellular senescence, a cell fate characterized by cell-cycle arrest and flat morphology. Oncogenic signaling can also induce cellular senescence which has been termed oncogene-induced senescence (OIS). Senescent cells display a pro-inflammatory phenotype which has been called the senescence-associated secretory phenotype (SASP). The secretomes associated with SASP contain colony-stimulating factors and chemokines which stimulate the generation of myeloid-derived suppressor cells (MDSC) by enhancing myelopoiesis in bone marrow and spleen. Enhanced myelopoiesis and increased level of MDSCs have been observed in bone marrow, spleen, and blood in both tumor-bearing and aged mice. Immunosuppressive MDSCs are recruited via chemotaxis into inflamed tissues where they proliferate and consequently suppress acute inflammatory reactions by inhibiting the functions of distinct components of innate and adaptive immunity. For instance, MDSCs stimulate the activity of immunosuppressive regulatory T-cells (Tregs). They also increase the expression of amino acid catabolizing enzymes and the secretion of anti-inflammatory cytokines, e.g. IL-10 and TGF-β, and reactive oxygen species (ROS). On the other hand, the accumulation of MDSCs into tissues exerts harmful effects in chronic pathological disorders, e.g. tumors and many age-related diseases, since the immunosuppression induced by MDSCs impairs the clearance of senescent and cancer cells and also disturbs the maintenance of energy metabolism and tissue proteostasis. The co-operation between senescent cells and immunosuppressive MDSCs regulates not only tumorigenesis and chronic inflammatory disorders but it also might promote inflammaging during the aging process.
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