Immunosenescence and immunogenetics of human longevity

R. Ostan, L. Bucci, M. Capri, S. Salvioli, M. Scurti, E. Pini, D. Monti, C. Franceschi

Research output: Contribution to journalArticle

Abstract

At present, individuals can live up to 80-120 years, a time much longer than that of our ancestors, as a consequence of the improvements in life conditions and medical care. Thus, the human immune system has to cope with a lifelong and evolutionarily unpredicted exposure to a variety of antigens, which are at the basis of profound age-related changes globally indicated as immunosenescence, a multifaceted phenomenon that increases morbidity and mortality due to infections and age-related pathologies. The major changes occurring during immunosenescence are the result of the accumulation of cellular, molecular defects and involutive phenomena (such as thymic involution) occurring concomitantly to a hyperstimulation of both innate and adaptive immunity (accumulation of expanded clones of memory and effector T cells, shrinkage of the T cell receptor repertoire, progressive activation of macrophages), and resulting in a low-grade, chronic state of inflammation defined as inflammaging. It is unknown whether inflammaging, which represents a risk factor for most age-related pathologies, is a cause or rather an effect of the aging process. In this complex scenario, the role of genetic background likely represents a fundamental variable to attain successful aging and longevity. Accordingly, centenarians seem to be equipped with gene variants that allow them to optimize the balance between pro- and anti-inflammatory molecules, and thus to minimize the effects of the lifelong exposure to environmental insults and stressors. The remarkable features of the genetics of aging and longevity are reviewed, stressing the unexpected and unusual results obtained regarding such a postreproductive type of genetics.

Original languageEnglish
Pages (from-to)224-240
Number of pages17
JournalNeuroImmunoModulation
Volume15
Issue number4-6
DOIs
Publication statusPublished - Nov 2008

Fingerprint

Immunogenetics
Pathology
Macrophage Activation
Environmental Exposure
Adaptive Immunity
T-Cell Antigen Receptor
Innate Immunity
Immune System
Anti-Inflammatory Agents
Clone Cells
Inflammation
Morbidity
T-Lymphocytes
Antigens
Mortality
Infection
Genes
Immunosenescence
Genetic Background

Keywords

  • Centenarians
  • Immunogenetics
  • Immunosenescence
  • Inflammaging
  • Longevity

ASJC Scopus subject areas

  • Endocrinology
  • Immunology
  • Endocrine and Autonomic Systems
  • Neurology

Cite this

Ostan, R., Bucci, L., Capri, M., Salvioli, S., Scurti, M., Pini, E., ... Franceschi, C. (2008). Immunosenescence and immunogenetics of human longevity. NeuroImmunoModulation, 15(4-6), 224-240. https://doi.org/10.1159/000156466

Immunosenescence and immunogenetics of human longevity. / Ostan, R.; Bucci, L.; Capri, M.; Salvioli, S.; Scurti, M.; Pini, E.; Monti, D.; Franceschi, C.

In: NeuroImmunoModulation, Vol. 15, No. 4-6, 11.2008, p. 224-240.

Research output: Contribution to journalArticle

Ostan, R, Bucci, L, Capri, M, Salvioli, S, Scurti, M, Pini, E, Monti, D & Franceschi, C 2008, 'Immunosenescence and immunogenetics of human longevity', NeuroImmunoModulation, vol. 15, no. 4-6, pp. 224-240. https://doi.org/10.1159/000156466
Ostan R, Bucci L, Capri M, Salvioli S, Scurti M, Pini E et al. Immunosenescence and immunogenetics of human longevity. NeuroImmunoModulation. 2008 Nov;15(4-6):224-240. https://doi.org/10.1159/000156466
Ostan, R. ; Bucci, L. ; Capri, M. ; Salvioli, S. ; Scurti, M. ; Pini, E. ; Monti, D. ; Franceschi, C. / Immunosenescence and immunogenetics of human longevity. In: NeuroImmunoModulation. 2008 ; Vol. 15, No. 4-6. pp. 224-240.
@article{1b12e12d6e50432a9bed249faee0a264,
title = "Immunosenescence and immunogenetics of human longevity",
abstract = "At present, individuals can live up to 80-120 years, a time much longer than that of our ancestors, as a consequence of the improvements in life conditions and medical care. Thus, the human immune system has to cope with a lifelong and evolutionarily unpredicted exposure to a variety of antigens, which are at the basis of profound age-related changes globally indicated as immunosenescence, a multifaceted phenomenon that increases morbidity and mortality due to infections and age-related pathologies. The major changes occurring during immunosenescence are the result of the accumulation of cellular, molecular defects and involutive phenomena (such as thymic involution) occurring concomitantly to a hyperstimulation of both innate and adaptive immunity (accumulation of expanded clones of memory and effector T cells, shrinkage of the T cell receptor repertoire, progressive activation of macrophages), and resulting in a low-grade, chronic state of inflammation defined as inflammaging. It is unknown whether inflammaging, which represents a risk factor for most age-related pathologies, is a cause or rather an effect of the aging process. In this complex scenario, the role of genetic background likely represents a fundamental variable to attain successful aging and longevity. Accordingly, centenarians seem to be equipped with gene variants that allow them to optimize the balance between pro- and anti-inflammatory molecules, and thus to minimize the effects of the lifelong exposure to environmental insults and stressors. The remarkable features of the genetics of aging and longevity are reviewed, stressing the unexpected and unusual results obtained regarding such a postreproductive type of genetics.",
keywords = "Centenarians, Immunogenetics, Immunosenescence, Inflammaging, Longevity",
author = "R. Ostan and L. Bucci and M. Capri and S. Salvioli and M. Scurti and E. Pini and D. Monti and C. Franceschi",
year = "2008",
month = "11",
doi = "10.1159/000156466",
language = "English",
volume = "15",
pages = "224--240",
journal = "NeuroImmunoModulation",
issn = "1021-7401",
publisher = "S. Karger AG",
number = "4-6",

}

TY - JOUR

T1 - Immunosenescence and immunogenetics of human longevity

AU - Ostan, R.

AU - Bucci, L.

AU - Capri, M.

AU - Salvioli, S.

AU - Scurti, M.

AU - Pini, E.

AU - Monti, D.

AU - Franceschi, C.

PY - 2008/11

Y1 - 2008/11

N2 - At present, individuals can live up to 80-120 years, a time much longer than that of our ancestors, as a consequence of the improvements in life conditions and medical care. Thus, the human immune system has to cope with a lifelong and evolutionarily unpredicted exposure to a variety of antigens, which are at the basis of profound age-related changes globally indicated as immunosenescence, a multifaceted phenomenon that increases morbidity and mortality due to infections and age-related pathologies. The major changes occurring during immunosenescence are the result of the accumulation of cellular, molecular defects and involutive phenomena (such as thymic involution) occurring concomitantly to a hyperstimulation of both innate and adaptive immunity (accumulation of expanded clones of memory and effector T cells, shrinkage of the T cell receptor repertoire, progressive activation of macrophages), and resulting in a low-grade, chronic state of inflammation defined as inflammaging. It is unknown whether inflammaging, which represents a risk factor for most age-related pathologies, is a cause or rather an effect of the aging process. In this complex scenario, the role of genetic background likely represents a fundamental variable to attain successful aging and longevity. Accordingly, centenarians seem to be equipped with gene variants that allow them to optimize the balance between pro- and anti-inflammatory molecules, and thus to minimize the effects of the lifelong exposure to environmental insults and stressors. The remarkable features of the genetics of aging and longevity are reviewed, stressing the unexpected and unusual results obtained regarding such a postreproductive type of genetics.

AB - At present, individuals can live up to 80-120 years, a time much longer than that of our ancestors, as a consequence of the improvements in life conditions and medical care. Thus, the human immune system has to cope with a lifelong and evolutionarily unpredicted exposure to a variety of antigens, which are at the basis of profound age-related changes globally indicated as immunosenescence, a multifaceted phenomenon that increases morbidity and mortality due to infections and age-related pathologies. The major changes occurring during immunosenescence are the result of the accumulation of cellular, molecular defects and involutive phenomena (such as thymic involution) occurring concomitantly to a hyperstimulation of both innate and adaptive immunity (accumulation of expanded clones of memory and effector T cells, shrinkage of the T cell receptor repertoire, progressive activation of macrophages), and resulting in a low-grade, chronic state of inflammation defined as inflammaging. It is unknown whether inflammaging, which represents a risk factor for most age-related pathologies, is a cause or rather an effect of the aging process. In this complex scenario, the role of genetic background likely represents a fundamental variable to attain successful aging and longevity. Accordingly, centenarians seem to be equipped with gene variants that allow them to optimize the balance between pro- and anti-inflammatory molecules, and thus to minimize the effects of the lifelong exposure to environmental insults and stressors. The remarkable features of the genetics of aging and longevity are reviewed, stressing the unexpected and unusual results obtained regarding such a postreproductive type of genetics.

KW - Centenarians

KW - Immunogenetics

KW - Immunosenescence

KW - Inflammaging

KW - Longevity

UR - http://www.scopus.com/inward/record.url?scp=57149086454&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=57149086454&partnerID=8YFLogxK

U2 - 10.1159/000156466

DO - 10.1159/000156466

M3 - Article

C2 - 19047800

AN - SCOPUS:57149086454

VL - 15

SP - 224

EP - 240

JO - NeuroImmunoModulation

JF - NeuroImmunoModulation

SN - 1021-7401

IS - 4-6

ER -