About: Abstract In early life as well as in late life, the immune system is dysfunctional. During early infancy, innate as well as adaptive immune cells are immature, immune memory has not been built, and regulatory pathways that maintain tolerance dominate. Throughout life, the adult human systems face the challenge of maintaining immune cell and population homeostasis while facing declining regenerative capacity and constant exogenous assaults. Failure of homeostatic mechanisms, together with age-acquired cellular defects, leads to the complex embodiment of immunosenescence that combines ineffective immune responses to infection and vaccination with constitutive production of inflammatory mediators and increased risk of autoimmunity.

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About: Abstract In early life as well as in late life, the immune system is dysfunctional. During early infancy, innate as well as adaptive immune cells are immature, immune memory has not been built, and regulatory pathways that maintain tolerance dominate. Throughout life, the adult human systems face the challenge of maintaining immune cell and population homeostasis while facing declining regenerative capacity and constant exogenous assaults. Failure of homeostatic mechanisms, together with age-acquired cellular defects, leads to the complex embodiment of immunosenescence that combines ineffective immune responses to infection and vaccination with constitutive production of inflammatory mediators and increased risk of autoimmunity. Goto Sponge NotDistinct Permalink

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type	abstract
value	Abstract In early life as well as in late life, the immune system is dysfunctional. During early infancy, innate as well as adaptive immune cells are immature, immune memory has not been built, and regulatory pathways that maintain tolerance dominate. Throughout life, the adult human systems face the challenge of maintaining immune cell and population homeostasis while facing declining regenerative capacity and constant exogenous assaults. Failure of homeostatic mechanisms, together with age-acquired cellular defects, leads to the complex embodiment of immunosenescence that combines ineffective immune responses to infection and vaccination with constitutive production of inflammatory mediators and increased risk of autoimmunity.
part of	38 Immune Deficiencies at the Extremes of Age
is abstract of	38 Immune Deficiencies at the Extremes of Age

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