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The Role of CMV in Immunosenescence

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The Ageing Immune System and Health

Abstract

The term “immunosenescence” is commonly taken to mean age-associated changes in immune parameters hypothesized to contribute to increased susceptibility and severity of the older adult to infectious disease, autoimmunity and cancer. In humans, it is characterized by lower numbers and frequencies of naïve T and B cells and higher numbers and frequencies of late-differentiated T cells, especially CD8+ T cells, in the peripheral blood. The latter may be very noticeable, but intriguingly, only in people infected by human herpesvirus 5 (Cytomegalovirus, CMV). Almost all human studies have been cross-sectional, thus documenting differences between old and young populations, but not necessarily changes over time. Nonetheless, limited longitudinal studies have provided data consistent with gradually decreasing naïve T and B cells, and increasing late-differentiated T cells over time, and in rare instances associating these changes with increasing frailty and incipient mortality in the elderly. Low numbers of naïve cells render the aged highly susceptible to pathogens to which they have not been previously exposed, but are not otherwise associated with an “immune risk profile” predicting earlier mortality. Whether the accumulations of late-differentiated T cells driven primarily by CMV contribute to frailty and mortality or are only adaptive responses to the persistent virus remains controversial. Either way, there is currently little direct evidence that “immunosenescence” contributes to either autoimmunity or cancer in the aged. This chapter reviews some of the studies implicating CMV infection in immunosenescence and its consequences for ageing trajectories in humans.

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Abbreviations

CCR7:

Chemokine receptor 7

CMV:

Cytomegalovirus

DC:

Dendritic cell

γδ T cells:

Gamma-delta T cells

IE-1:

Immediate early protein 1

IFN:

Interferon

KLRG:

Killer lectin-like cell receptor G1

MHC:

Major histocompatibility complex

NK cell:

Natural killer cell

PBMC:

Peripheral blood mononuclear cells

pp65:

Tegument protein

TLR:

Toll-like receptor

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Acknowledgments

This work was supported by the European Commission under Grant Agreement FP7 259679, Integrated research on developmental determinants of ageing and longevity, “IDEAL” and by an unrestricted educational grant from the Croeni Foundation (to GP).

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Authors and Affiliations

  1. Max Planck Institute for Human Development, Lentzeallee 94, 14195, Berlin, Germany

    Ludmila Müller

  2. Institute of Medical Virology, University of Tübingen, Tübingen, Germany

    Klaus Hamprecht

  3. Center for Medical Research, University of Tübingen, Waldhörnlestr. 22, 72072, Tübingen, Germany

    Graham Pawelec

  4. Division of Cancer Studies, Faculty of Life Sciences and Medicine, King’s College London, London, UK

    Graham Pawelec

  5. The John van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Nottingham, UK

    Graham Pawelec

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  1. Ludmila Müller
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Correspondence to Graham Pawelec .

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Editors and Affiliations

  1. Department of Microbiology, Immunology and Parasitology UNIFESP Federal University of São Paulo, Sao Paulo, São Paulo, Brazil

    Valquiria Bueno

  2. MRC-ARUK Centre for Musculoskeletal Ageing Research, Institute of Inflammation and Ageing Birmingham University Medical School Birmingham, Birmingham, United Kingdom

    Janet M. Lord

  3. Institute of Inflammation and Ageing, University of Birmingham University of Birmingham Research Laboratories, Birmingham, United Kingdom

    Thomas A. Jackson

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Müller, L., Hamprecht, K., Pawelec, G. (2017). The Role of CMV in Immunosenescence. In: Bueno, V., Lord, J., Jackson, T. (eds) The Ageing Immune System and Health. Springer, Cham. https://doi.org/10.1007/978-3-319-43365-3_4

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