We are analyzing https://link.springer.com/article/10.1007/s00109-021-02123-w.

Title:
Immunosuppressive network promotes immunosenescence associated with aging and chronic inflammatory conditions | Journal of Molecular Medicine
Description:
The functional competence of the immune system gradually declines with aging, a process called immunosenescence. The age-related remodelling of the immune system affects both adaptive and innate immunity. In particular, a chronic low-grade inflammation, termed inflammaging, is associated with the aging process. Immunosenescence not only is present in inflammaging state, but it also occurs in several pathological conditions in conjunction with chronic inflammation. It is known that persistent inflammation stimulates a counteracting compensatory immunosuppression intended to protect host tissues. Inflammatory mediators enhance myelopoiesis and induce the generation of immature myeloid-derived suppressor cells (MDSC) which in mutual cooperation stimulates the immunosuppressive network. Immunosuppressive cells, especially MDSCs, regulatory T cells (Treg), and M2 macrophages produce immunosuppressive factors, e.g., TGF-β, IL-10, ROS, arginase-1 (ARG1), and indoleamine 2,3-dioxygenase (IDO), which suppress the functions of CD4/CD8T and B cells as well as macrophages, natural killer (NK) cells, and dendritic cells. The immunosuppressive armament (i) inhibits the development and proliferation of immune cells, (ii) decreases the cytotoxic activity of CD8T and NK cells, (iii) prevents antigen presentation and antibody production, and (iv) suppresses responsiveness to inflammatory mediators. These phenotypes are the hallmarks of immunosenescence. Immunosuppressive factors are able to control the chromatin landscape, and thus, it seems that the immunosenescence state is epigenetically regulated.
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Keywords {🔍}

cells, pubmed, article, google, scholar, cas, aging, immune, immunosenescence, cell, central, senescence, human, immunosuppressive, immunol, macrophages, senescent, mdscs, inflammatory, agerelated, tgfβ, process, state, suppressor, tregs, mouse, regulatory, activity, increased, epigenetic, signaling, cellular, chronic, inflammation, activation, expression, reported, immunosuppression, myeloidderived, induced, function, functions, mice, instance, cytokines, demonstrated, cancer, network, production, sasp,

Topics {✒️}

sars-cov-2 virus-induced infection membrane-bound tgf-β1 proteins age-related myeloid-biased dominance important smad-independent target sestrin-mapk activation complex transforming growth factor-β p53-inducible stress-sensing proteins article download pdf sars-cov2 virus induced sa-β-gal-positive cells compensatory anti-inflammatory syndrome β-galactosidase-positive macrophage accumulation membrane-bound tgf-β myeloid-derived suppressor cells membrane-bound tgf-β1 ampk-dach1-cxcl1 axis martinez de toda kinase p38 activated tgf-β-induced epigenetic mechanisms tgf-β1 gene promoter b-cell depletion reactivates cyclin-dependent kinase inhibitors traf/tak1 signaling axis decreased tnf-α synthesis tgf-β/nkg2d complex [132] tgf-β signaling pathways con a-induced hepatitis muscle-derived nitric oxide age-related immune deficiency tgf-β exposure upregulates chronic low-grade inflammation low-grade chronic inflammation amino acid-catabolizing enzymes c57bl/6j geriatric mice tgf-β/smad tumor-derived γδ regulatory peripheral blood t-cells hla-e-mediated nk article salminen age-related oxidative stress pro-inflammatory sasp secretome colony stimulating factors tumor-expressed ido recruits chronic inflammation-induced immunosuppression cell-mediated immune responses human antigen-specific cd4+ target anti-inflammatory genes dna methylation-based biomarkers tgf-β exposure reduces acute inflammatory responses

Questions {❓}

Aiello A, Farzaneh F, Candore G, Caruso C, Davinelli S, Gambino CM, Ligotti ME, Zareian N, Accardi G (2019) Immunosenescence and its hallmarks: how to oppose aging strategically?
Akbar AN, Henson SM (2011) Are senescence and exhaustion intertwined or unrelated processes that compromise immunity?
Bauer ME, Teixeira AL (2019) Inflammation in psychiatric disorders: what comes first?
Fulop T, Larbi A, Dupuis G, Le Page A, Frost EH, Cohen AA, Witkowski JM, Franceschi C (2018) Immunosenescence and inflamm-aging as two sides of the same coin: friends or foes?
Future perspectives: to rejuvenate or to prevent immunosuppression?
Pawelec G (2020) The human immunosenescence phenotype: does it exist?
Sanchez-Correa B, Campos C, Pera A, Bergua JM, Arcos MJ, Banas H, Casado JG, Morgado S, Duran E, Solana R et al (2016) Natural killer cell immunosenescence in acute myeloid leukaemia patients: new targets for immunotherapeutic strategies?

Schema {🗺️}

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         headline:Immunosuppressive network promotes immunosenescence associated with aging and chronic inflammatory conditions
         description:The functional competence of the immune system gradually declines with aging, a process called immunosenescence. The age-related remodelling of the immune system affects both adaptive and innate immunity. In particular, a chronic low-grade inflammation, termed inflammaging, is associated with the aging process. Immunosenescence not only is present in inflammaging state, but it also occurs in several pathological conditions in conjunction with chronic inflammation. It is known that persistent inflammation stimulates a counteracting compensatory immunosuppression intended to protect host tissues. Inflammatory mediators enhance myelopoiesis and induce the generation of immature myeloid-derived suppressor cells (MDSC) which in mutual cooperation stimulates the immunosuppressive network. Immunosuppressive cells, especially MDSCs, regulatory T cells (Treg), and M2 macrophages produce immunosuppressive factors, e.g., TGF-β, IL-10, ROS, arginase-1 (ARG1), and indoleamine 2,3-dioxygenase (IDO), which suppress the functions of CD4/CD8T and B cells as well as macrophages, natural killer (NK) cells, and dendritic cells. The immunosuppressive armament (i) inhibits the development and proliferation of immune cells, (ii) decreases the cytotoxic activity of CD8T and NK cells, (iii) prevents antigen presentation and antibody production, and (iv) suppresses responsiveness to inflammatory mediators. These phenotypes are the hallmarks of immunosenescence. Immunosuppressive factors are able to control the chromatin landscape, and thus, it seems that the immunosenescence state is epigenetically regulated.
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      headline:Immunosuppressive network promotes immunosenescence associated with aging and chronic inflammatory conditions
      description:The functional competence of the immune system gradually declines with aging, a process called immunosenescence. The age-related remodelling of the immune system affects both adaptive and innate immunity. In particular, a chronic low-grade inflammation, termed inflammaging, is associated with the aging process. Immunosenescence not only is present in inflammaging state, but it also occurs in several pathological conditions in conjunction with chronic inflammation. It is known that persistent inflammation stimulates a counteracting compensatory immunosuppression intended to protect host tissues. Inflammatory mediators enhance myelopoiesis and induce the generation of immature myeloid-derived suppressor cells (MDSC) which in mutual cooperation stimulates the immunosuppressive network. Immunosuppressive cells, especially MDSCs, regulatory T cells (Treg), and M2 macrophages produce immunosuppressive factors, e.g., TGF-β, IL-10, ROS, arginase-1 (ARG1), and indoleamine 2,3-dioxygenase (IDO), which suppress the functions of CD4/CD8T and B cells as well as macrophages, natural killer (NK) cells, and dendritic cells. The immunosuppressive armament (i) inhibits the development and proliferation of immune cells, (ii) decreases the cytotoxic activity of CD8T and NK cells, (iii) prevents antigen presentation and antibody production, and (iv) suppresses responsiveness to inflammatory mediators. These phenotypes are the hallmarks of immunosenescence. Immunosuppressive factors are able to control the chromatin landscape, and thus, it seems that the immunosenescence state is epigenetically regulated.
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         Alzheimer’s
         Cellular senescence
         Immune tolerance
         Immunosuppression
         Kynurenine
         Molecular Medicine
         Human Genetics
         Internal Medicine
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