We are analyzing https://link.springer.com/article/10.1186/s12979-020-0173-8.

Title:
Contributions of Age-Related Thymic Involution to Immunosenescence and Inflammaging | Immunity & Ageing
Description:
Immune system aging is characterized by the paradox of immunosenescence (insufficiency) and inflammaging (over-reaction), which incorporate two sides of the same coin, resulting in immune disorder. Immunosenescence refers to disruption in the structural architecture of immune organs and dysfunction in immune responses, resulting from both aged innate and adaptive immunity. Inflammaging, described as a chronic, sterile, systemic inflammatory condition associated with advanced age, is mainly attributed to somatic cellular senescence-associated secretory phenotype (SASP) and age-related autoimmune predisposition. However, the inability to reduce senescent somatic cells (SSCs), because of immunosenescence, exacerbates inflammaging. Age-related adaptive immune system deviations, particularly altered T cell function, are derived from age-related thymic atrophy or involution, a hallmark of thymic aging. Recently, there have been major developments in understanding how age-related thymic involution contributes to inflammaging and immunosenescence at the cellular and molecular levels, including genetic and epigenetic regulation, as well as developments of many potential rejuvenation strategies. Herein, we discuss the research progress uncovering how age-related thymic involution contributes to immunosenescence and inflammaging, as well as their intersection. We also describe how T cell adaptive immunity mediates inflammaging and plays a crucial role in the progression of age-related neurological and cardiovascular diseases, as well as cancer. We then briefly outline the underlying cellular and molecular mechanisms of age-related thymic involution, and finally summarize potential rejuvenation strategies to restore aged thymic function.
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Keywords {🔍}

pubmed, google, scholar, article, cas, cells, thymic, cell, central, thymus, aged, agerelated, aging, immunol, immune, involution, immunosenescence, inflammaging, cancer, increased, treg, mice, function, development, regulatory, foxn, selection, expression, growth, role, rev, system, senescence, negative, tumor, stem, cellular, diseases, age, reduced, tcr, disease, studies, peripheral, mouse, nat, generation, inflammation, factor, young,

Topics {✒️}

bone-marrow haematopoietic-stem-cell niches ifn-γ-producing th1 cells reduce age-related multi-morbidity il-17a-producing th17 cells promotes t-cell recovery article download pdf n-terminal extracellular domain myeloid-derived suppressor cells serum-derived extracellular vesicles basal inflammatory state abnormal nf-kappab2 signaling age-related thymic impairments durable cell-cycle arrest pro-inflammatory th1 phenotype ifn-gamma-dependent activation human psc-derived foxn1 age-related thymic involution age-related autoimmune predisposition utilized genetically-based methods tec-autonomous factor foxn1 nan-ping peter weng nih/niaid grant r01ai121147 dong-ming su unbalanced anti-tumour response age-related thymic atrophy extensive age-related alterations dna-damage signaling cascades central nervous system abetappswe/ps1de9 transgenic mice age-related neurodegenerative diseases cell–mediated autoimmune responses cell ifn-gamma expression th17 cell-mediated neuroinflammation central tolerance establishment establish central tolerance pmhc-ii ligand expression mendes-da-cruz da postnatal tissue-specific disruption chronic pro-inflammatory status tcaf3-specific treg cells negatively impact antigen-specific amplified oligo-clonal expansion age-related immune dysregulation age-related decreased thymopoiesis tec-based cellular therapy blood-brain barrier integrity central tolerance induction p53 tumor suppressor anti-apoptotic pathways involve tcr signaling received

Questions {❓}

Age and immunity: What is “immunosenescence”?
Can physical activity ameliorate immunosenescence and thereby reduce age-related multi-morbidity?
Immunosenescence and Inflamm-Aging As Two Sides of the Same Coin: Friends or Foes?
Immunosenescence: a product of the environment?
Immunosenescence: what does it mean to health outcomes in older adults?
Inflammation and cancer: back to Virchow?
Is ageing associated with a shift in the balance between Type 1 and Type 2 cytokines in humans?
Mechanisms shaping the naive T cell repertoire in the elderly - thymic involution or peripheral homeostatic proliferation?
Therefore, why is the increased or unchanged proportion of Treg cells unable to successfully manage self-reactivity in the elderly?

Schema {🗺️}

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         description:Immune system aging is characterized by the paradox of immunosenescence (insufficiency) and inflammaging (over-reaction), which incorporate two sides of the same coin, resulting in immune disorder. Immunosenescence refers to disruption in the structural architecture of immune organs and dysfunction in immune responses, resulting from both aged innate and adaptive immunity. Inflammaging, described as a chronic, sterile, systemic inflammatory condition associated with advanced age, is mainly attributed to somatic cellular senescence-associated secretory phenotype (SASP) and age-related autoimmune predisposition. However, the inability to reduce senescent somatic cells (SSCs), because of immunosenescence, exacerbates inflammaging. Age-related adaptive immune system deviations, particularly altered T cell function, are derived from age-related thymic atrophy or involution, a hallmark of thymic aging. Recently, there have been major developments in understanding how age-related thymic involution contributes to inflammaging and immunosenescence at the cellular and molecular levels, including genetic and epigenetic regulation, as well as developments of many potential rejuvenation strategies. Herein, we discuss the research progress uncovering how age-related thymic involution contributes to immunosenescence and inflammaging, as well as their intersection. We also describe how T cell adaptive immunity mediates inflammaging and plays a crucial role in the progression of age-related neurological and cardiovascular diseases, as well as cancer. We then briefly outline the underlying cellular and molecular mechanisms of age-related thymic involution, and finally summarize potential rejuvenation strategies to restore aged thymic function.
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      description:Immune system aging is characterized by the paradox of immunosenescence (insufficiency) and inflammaging (over-reaction), which incorporate two sides of the same coin, resulting in immune disorder. Immunosenescence refers to disruption in the structural architecture of immune organs and dysfunction in immune responses, resulting from both aged innate and adaptive immunity. Inflammaging, described as a chronic, sterile, systemic inflammatory condition associated with advanced age, is mainly attributed to somatic cellular senescence-associated secretory phenotype (SASP) and age-related autoimmune predisposition. However, the inability to reduce senescent somatic cells (SSCs), because of immunosenescence, exacerbates inflammaging. Age-related adaptive immune system deviations, particularly altered T cell function, are derived from age-related thymic atrophy or involution, a hallmark of thymic aging. Recently, there have been major developments in understanding how age-related thymic involution contributes to inflammaging and immunosenescence at the cellular and molecular levels, including genetic and epigenetic regulation, as well as developments of many potential rejuvenation strategies. Herein, we discuss the research progress uncovering how age-related thymic involution contributes to immunosenescence and inflammaging, as well as their intersection. We also describe how T cell adaptive immunity mediates inflammaging and plays a crucial role in the progression of age-related neurological and cardiovascular diseases, as well as cancer. We then briefly outline the underlying cellular and molecular mechanisms of age-related thymic involution, and finally summarize potential rejuvenation strategies to restore aged thymic function.
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         Antibodies
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