Is immunosenescence infectious?

Calogero Caruso, Anders Wikby, Beatrix Grubeck-Loebenstein, Rita Effros, Arne Akbar, Graham Pawelec

Risultato della ricerca: Article

202 Citazioni (Scopus)

Abstract

Herpes viruses are endemic. Once established, the virus is never eliminated but persists throughout life. The fraction of infected individuals gradually increases with age, such that the majority of elderly people are cytomegalovirus (CMV)(+), Epstein-Barr virus (EBV)(+) and Varicella(+). Clinically relevant reactivation of Varicella causes painful shingles; CMV reactivation can cause fatal pneumonia. Overt reactivation, even in the very elderly, occurs only in immunocompromised individuals; however, the necessity for maintaining immunity to these viruses is costly. We argue that this cost is not only reflected in the requirement for continuous immunosurveillance against these viruses but, more importantly, results in a re-configuration of T-cell immunity due to the accumulation of dysfunctional virus-specific cells, which fail to be eliminated from the system. Thus, we hypothesize that it is the chronic antigenic stimulation by CMV (and possibly other persisting antigens) that leads to an increasing prevalence of senescent, dysfunctional T cells, and therefore contributes to more general alterations in the immune system, which are associated with earlier mortality.
Lingua originaleEnglish
pagine (da-a)406-410
RivistaTrends in Immunology
Volume25
Stato di pubblicazionePublished - 2004

Fingerprint

Viruses
Cytomegalovirus
Chickenpox
Immunity
T-Lymphocytes
Immunologic Monitoring
Herpes Zoster
Human Herpesvirus 4
Immune System
Pneumonia
Immunosenescence
Antigens
Costs and Cost Analysis
Mortality

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cita questo

Caruso, C., Wikby, A., Grubeck-Loebenstein, B., Effros, R., Akbar, A., & Pawelec, G. (2004). Is immunosenescence infectious? Trends in Immunology, 25, 406-410.

Is immunosenescence infectious? / Caruso, Calogero; Wikby, Anders; Grubeck-Loebenstein, Beatrix; Effros, Rita; Akbar, Arne; Pawelec, Graham.

In: Trends in Immunology, Vol. 25, 2004, pag. 406-410.

Risultato della ricerca: Article

Caruso, C, Wikby, A, Grubeck-Loebenstein, B, Effros, R, Akbar, A & Pawelec, G 2004, 'Is immunosenescence infectious?', Trends in Immunology, vol. 25, pagg. 406-410.
Caruso C, Wikby A, Grubeck-Loebenstein B, Effros R, Akbar A, Pawelec G. Is immunosenescence infectious? Trends in Immunology. 2004;25:406-410.
Caruso, Calogero ; Wikby, Anders ; Grubeck-Loebenstein, Beatrix ; Effros, Rita ; Akbar, Arne ; Pawelec, Graham. / Is immunosenescence infectious?. In: Trends in Immunology. 2004 ; Vol. 25. pagg. 406-410.
@article{f8b99e85f2fe4317bf3a4e6426138a40,
title = "Is immunosenescence infectious?",
abstract = "Herpes viruses are endemic. Once established, the virus is never eliminated but persists throughout life. The fraction of infected individuals gradually increases with age, such that the majority of elderly people are cytomegalovirus (CMV)(+), Epstein-Barr virus (EBV)(+) and Varicella(+). Clinically relevant reactivation of Varicella causes painful shingles; CMV reactivation can cause fatal pneumonia. Overt reactivation, even in the very elderly, occurs only in immunocompromised individuals; however, the necessity for maintaining immunity to these viruses is costly. We argue that this cost is not only reflected in the requirement for continuous immunosurveillance against these viruses but, more importantly, results in a re-configuration of T-cell immunity due to the accumulation of dysfunctional virus-specific cells, which fail to be eliminated from the system. Thus, we hypothesize that it is the chronic antigenic stimulation by CMV (and possibly other persisting antigens) that leads to an increasing prevalence of senescent, dysfunctional T cells, and therefore contributes to more general alterations in the immune system, which are associated with earlier mortality.",
author = "Calogero Caruso and Anders Wikby and Beatrix Grubeck-Loebenstein and Rita Effros and Arne Akbar and Graham Pawelec",
year = "2004",
language = "English",
volume = "25",
pages = "406--410",
journal = "Trends in Immunology",
issn = "1471-4906",
publisher = "Elsevier Limited",

}

TY - JOUR

T1 - Is immunosenescence infectious?

AU - Caruso, Calogero

AU - Wikby, Anders

AU - Grubeck-Loebenstein, Beatrix

AU - Effros, Rita

AU - Akbar, Arne

AU - Pawelec, Graham

PY - 2004

Y1 - 2004

N2 - Herpes viruses are endemic. Once established, the virus is never eliminated but persists throughout life. The fraction of infected individuals gradually increases with age, such that the majority of elderly people are cytomegalovirus (CMV)(+), Epstein-Barr virus (EBV)(+) and Varicella(+). Clinically relevant reactivation of Varicella causes painful shingles; CMV reactivation can cause fatal pneumonia. Overt reactivation, even in the very elderly, occurs only in immunocompromised individuals; however, the necessity for maintaining immunity to these viruses is costly. We argue that this cost is not only reflected in the requirement for continuous immunosurveillance against these viruses but, more importantly, results in a re-configuration of T-cell immunity due to the accumulation of dysfunctional virus-specific cells, which fail to be eliminated from the system. Thus, we hypothesize that it is the chronic antigenic stimulation by CMV (and possibly other persisting antigens) that leads to an increasing prevalence of senescent, dysfunctional T cells, and therefore contributes to more general alterations in the immune system, which are associated with earlier mortality.

AB - Herpes viruses are endemic. Once established, the virus is never eliminated but persists throughout life. The fraction of infected individuals gradually increases with age, such that the majority of elderly people are cytomegalovirus (CMV)(+), Epstein-Barr virus (EBV)(+) and Varicella(+). Clinically relevant reactivation of Varicella causes painful shingles; CMV reactivation can cause fatal pneumonia. Overt reactivation, even in the very elderly, occurs only in immunocompromised individuals; however, the necessity for maintaining immunity to these viruses is costly. We argue that this cost is not only reflected in the requirement for continuous immunosurveillance against these viruses but, more importantly, results in a re-configuration of T-cell immunity due to the accumulation of dysfunctional virus-specific cells, which fail to be eliminated from the system. Thus, we hypothesize that it is the chronic antigenic stimulation by CMV (and possibly other persisting antigens) that leads to an increasing prevalence of senescent, dysfunctional T cells, and therefore contributes to more general alterations in the immune system, which are associated with earlier mortality.

UR - http://hdl.handle.net/10447/2746

M3 - Article

VL - 25

SP - 406

EP - 410

JO - Trends in Immunology

JF - Trends in Immunology

SN - 1471-4906

ER -