We are analyzing https://link.springer.com/article/10.1007/s00109-020-01988-7.

Title:
Increased immunosuppression impairs tissue homeostasis with aging and age-related diseases | Journal of Molecular Medicine
Description:
Abstract Chronic low-grade inflammation is a common hallmark of the aging process and many age-related diseases. There is substantial evidence that persistent inflammation is associated with a compensatory anti-inflammatory response which prevents excessive tissue damage. Interestingly, the inflammatory state encountered with aging, called inflammaging, is associated with the anti-inflammaging process. The age-related activation of immunosuppressive network includes an increase in the numbers of myeloid-derived suppressor cells (MDSC), regulatory T cells (Treg), and macrophages (Mreg/M2c). Immunosuppressive cells secrete several anti-inflammatory cytokines, e.g., TGF-β and IL-10, as well as reactive oxygen and nitrogen species (ROS/RNS). Moreover, immunosuppressive cells suppress the function of effector immune cells by catabolizing l-arginine and tryptophan through the activation of arginase 1 (ARG1) and indoleamine 2,3-dioxygenase (IDO), respectively. Unfortunately, the immunosuppressive armament also induces harmful bystander effects in neighboring cells by impairing host tissue homeostasis. For instance, TGF-β signaling can trigger many age-related degenerative changes, e.g., cellular senescence, fibrosis, osteoporosis, muscle atrophy, and the degeneration of the extracellular matrix. In addition, changes in the levels of ROS, RNS, and the metabolites of the kynurenine pathway can impair tissue homeostasis. This review will examine in detail the harmful effects of the immunosuppressive cells on host tissues. It seems that this age-related immunosuppression prevents inflammatory damage but promotes the tissue degeneration associated with aging and age-related diseases. Key messages • Low-grade inflammation is associated with the aging process and age-related diseases. • Persistent inflammation activates compensatory immunosuppression with aging. • The numbers of immunosuppressive cells increase with aging and age-related diseases. • Immunosuppressive mechanisms evoke harmful bystander effects in host tissues. • Immunosuppression promotes tissue degeneration with aging and age-related diseases.
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Keywords {🔍}

pubmed, cells, google, scholar, cas, aging, tgfβ, central, immunosuppressive, signaling, cell, immune, tissues, inflammation, expression, agerelated, mdscs, activation, senescent, senescence, increased, immunosuppression, diseases, chronic, inflammatory, cytokines, immunol, tissue, role, process, regulatory, protein, mouse, cellular, amino, macrophages, instance, disease, responses, suppressor, human, antiinflammatory, ido, ros, tryptophan, fibrosis, effects, demonstrated, network, wang,

Topics {✒️}

gr-1+cd11b+myeloid-derived suppressor cells tgf-β/nf1/smad4-mediated suppression tgf-β-induced fibrogenic responses age-related low-grade inflammation life-threatening sirs/cars condition tgf-β1-induced myofiber atrophy age-related cardiomyocyte hypertrophy smad-dependent tgf-β signaling chronic low-grade inflammation myeloid-derived suppressor cell tgf-β-induced muscle atrophy anti-inflammatory cytokines tgf-β myeloid-derived suppressor cells nf-κb-dependent mechanism tissue-enriched anti-inflammatory cytokines transforming growth factor-β epithelial/endothelial-mesenchymal transition nf-κb-driven generation cyclin-dependent kinase inhibitors suppressed tgf-β signaling low-grade inflammation present myeloid-biased hscs superimposed compensatory anti-inflammatory syndrome nutrient-sensing protein kinase pro-inflammatory m1 subtype membrane-bound tgf-β1 pi3k/akt/mtor axis [142] muscle-derived nitric oxide article download pdf macrophage-specific chromatin signature tryptophan-derived 3-hydroxykynurenine stimulated il10-akt-mtor pathways van der loo c57bl/6j geriatric mice activated tgf-β signaling pi3k/akt/mtor pathway il10-driven stat3 signalling tissue-resident immune cells compensatory anti-inflammatory response endotoxin-induced lung inflammation secrete colony-stimulating factors tgf-β signaling stimulates age-related diseases elicit age-related oxidative stress cell–dependent antibody responses tgf-β signaling regulates tgf-β1 stimulates production myeloid-biased hsc proliferation eif2α-driven protein synthesis chronic inflammation-induced immunosuppression

Questions {❓}

Balk RA (2014) Systemic inflammatory response syndrome (SIRS): where did it come from and is it still relevant today?
Brown-Borg HM, Buffenstein R (2017) Cutting back on the essentials: can manipulating intake of specific amino acids modulate health and lifespan?
Is immunosuppression the driving force in the aging process?
Kaluzna-Czaplinska J, Gątarek P, Chirumbolo S, Chartrand MS, Björklund G (2019) How important is tryptophan in human health?
Lind M, Hayes A, Caprnda M, Petrovic D, Rodrigo L, Kruzliak P, Zulli A (2017) Inducible nitric oxide synthase: good or bad?
Mellor AL, Lemos H, Huang L (2017) Indoleamine 2,3-dioxygenase and tolerance: where are we now?
Tavernarakis N (2008) Ageing and the regulation of protein synthesis: a balancing act?

Schema {🗺️}

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         description:Chronic low-grade inflammation is a common hallmark of the aging process and many age-related diseases. There is substantial evidence that persistent inflammation is associated with a compensatory anti-inflammatory response which prevents excessive tissue damage. Interestingly, the inflammatory state encountered with aging, called inflammaging, is associated with the anti-inflammaging process. The age-related activation of immunosuppressive network includes an increase in the numbers of myeloid-derived suppressor cells (MDSC), regulatory T cells (Treg), and macrophages (Mreg/M2c). Immunosuppressive cells secrete several anti-inflammatory cytokines, e.g., TGF-β and IL-10, as well as reactive oxygen and nitrogen species (ROS/RNS). Moreover, immunosuppressive cells suppress the function of effector immune cells by catabolizing l-arginine and tryptophan through the activation of arginase 1 (ARG1) and indoleamine 2,3-dioxygenase (IDO), respectively. Unfortunately, the immunosuppressive armament also induces harmful bystander effects in neighboring cells by impairing host tissue homeostasis. For instance, TGF-β signaling can trigger many age-related degenerative changes, e.g., cellular senescence, fibrosis, osteoporosis, muscle atrophy, and the degeneration of the extracellular matrix. In addition, changes in the levels of ROS, RNS, and the metabolites of the kynurenine pathway can impair tissue homeostasis. This review will examine in detail the harmful effects of the immunosuppressive cells on host tissues. It seems that this age-related immunosuppression prevents inflammatory damage but promotes the tissue degeneration associated with aging and age-related diseases. • Low-grade inflammation is associated with the aging process and age-related diseases. • Persistent inflammation activates compensatory immunosuppression with aging. • The numbers of immunosuppressive cells increase with aging and age-related diseases. • Immunosuppressive mechanisms evoke harmful bystander effects in host tissues. • Immunosuppression promotes tissue degeneration with aging and age-related diseases.
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      headline:Increased immunosuppression impairs tissue homeostasis with aging and age-related diseases
      description:Chronic low-grade inflammation is a common hallmark of the aging process and many age-related diseases. There is substantial evidence that persistent inflammation is associated with a compensatory anti-inflammatory response which prevents excessive tissue damage. Interestingly, the inflammatory state encountered with aging, called inflammaging, is associated with the anti-inflammaging process. The age-related activation of immunosuppressive network includes an increase in the numbers of myeloid-derived suppressor cells (MDSC), regulatory T cells (Treg), and macrophages (Mreg/M2c). Immunosuppressive cells secrete several anti-inflammatory cytokines, e.g., TGF-β and IL-10, as well as reactive oxygen and nitrogen species (ROS/RNS). Moreover, immunosuppressive cells suppress the function of effector immune cells by catabolizing l-arginine and tryptophan through the activation of arginase 1 (ARG1) and indoleamine 2,3-dioxygenase (IDO), respectively. Unfortunately, the immunosuppressive armament also induces harmful bystander effects in neighboring cells by impairing host tissue homeostasis. For instance, TGF-β signaling can trigger many age-related degenerative changes, e.g., cellular senescence, fibrosis, osteoporosis, muscle atrophy, and the degeneration of the extracellular matrix. In addition, changes in the levels of ROS, RNS, and the metabolites of the kynurenine pathway can impair tissue homeostasis. This review will examine in detail the harmful effects of the immunosuppressive cells on host tissues. It seems that this age-related immunosuppression prevents inflammatory damage but promotes the tissue degeneration associated with aging and age-related diseases. • Low-grade inflammation is associated with the aging process and age-related diseases. • Persistent inflammation activates compensatory immunosuppression with aging. • The numbers of immunosuppressive cells increase with aging and age-related diseases. • Immunosuppressive mechanisms evoke harmful bystander effects in host tissues. • Immunosuppression promotes tissue degeneration with aging and age-related diseases.
      datePublished:2020-10-06T00:00:00Z
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         Alzheimer’s
         Immunometabolism
         Immunosenescence
         Nitric oxide
         Tissue degeneration
         Molecular Medicine
         Human Genetics
         Internal Medicine
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