Document Detail


Aging and immune function: molecular mechanisms to interventions.
MedLine Citation:
PMID:  20812785     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Abstract The immune system of an organism is an essential component of the defense mechanism aimed at combating pathogenic stress. Age-associated immune dysfunction, also dubbed "immune senescence," manifests as increased susceptibility to infections, increased onset and progression of autoimmune diseases, and onset of neoplasia. Over the years, extensive research has generated consensus in terms of the phenotypic and functional defects within the immune system in various organisms, including humans. Indeed, age-associated alterations such as thymic involution, T cell repertoire skewing, decreased ability to activate naïve T cells and to generate robust memory responses, have been shown to have a causative role in immune decline. Further, understanding the molecular mechanisms underlying the generation of proteotoxic stress, DNA damage response, modulation of ubiquitin proteasome pathway, and regulation of transcription factor NFκB activation, in immune decline, have paved the way to delineating signaling pathways that cross-talk and impact immune senescence. Given the role of the immune system in combating infections, its effectiveness with age may well be a marker of health and a predictor of longevity. It is therefore believed that a better understanding of the mechanisms underlying immune senescence will lead to an effective interventional strategy aimed at improving the health span of individuals. Antioxid. Redox Signal. 14, 1551-1585.
Authors:
Subramaniam Ponnappan; Usha Ponnappan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2011-01-08
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  14     ISSN:  1557-7716     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-22     Completed Date:  2012-02-08     Revised Date:  2012-04-16    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1551-85     Citation Subset:  IM    
Affiliation:
Department of Geriatrics, University of Arkansas for Medical Sciences, 4301 W. Markham, Little Rock, AR 72205, USA.
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MeSH Terms
Descriptor/Qualifier:
Aging*
Animals
DNA / immunology
Humans
Immune System / immunology*
MicroRNAs / immunology
NF-kappa B / immunology
Reactive Oxygen Species / immunology
T-Lymphocytes / immunology
Telomere / immunology
Grant Support
ID/Acronym/Agency:
AG025220/AG/NIA NIH HHS; AG030599/AG/NIA NIH HHS; AG13081/AG/NIA NIH HHS; R01 AG030599-05/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/MicroRNAs; 0/NF-kappa B; 0/Reactive Oxygen Species; 9007-49-2/DNA

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