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Scientific article
English

CD8+ T cells induce cachexia during chronic viral infection

Published inNature Immunology, vol. 20, no. 6, p. 701-710
Publication date2019
Abstract

Cachexia represents a leading cause of morbidity and mortality in various cancers, chronic inflammation and infections. Understanding of the mechanisms that drive cachexia has remained limited, especially for infection-associated cachexia (IAC). In the present paper we describe a model of reversible cachexia in mice with chronic viral infection and identify an essential role for CD8+ T cells in IAC. Cytokines linked to cancer-associated cachexia did not contribute to IAC. Instead, virus-specific CD8+ T cells caused morphologic and molecular changes in the adipose tissue, which led to depletion of lipid stores. These changes occurred at a time point that preceded the peak of the CD8+ T cell response and required T cell-intrinsic type I interferon signaling and antigen-specific priming. Our results link systemic antiviral immune responses to adipose-tissue remodeling and reveal an underappreciated role of CD8+ T cells in IAC.

Keywords
  • Adipose Tissue/diagnostic imaging/immunology/metabolism/virology
  • Animals
  • CD8-Positive T-Lymphocytes/immunology/metabolism
  • Cachexia/diagnostic imaging/etiology/metabolism/pathology
  • Chronic Disease
  • Cytokines/blood/metabolism
  • Female
  • Interferon Type I/metabolism
  • Lipid Metabolism
  • Lipolysis
  • Lymphocyte Activation/immunology
  • Lymphocytic choriomeningitis virus
  • Magnetic Resonance Imaging/methods
  • Male
  • Mice
  • Signal Transduction
  • Virus Diseases/complications/immunology/virology
Funding
  • European Commission - Crosstalk of Metabolism and Inflammation [677006]
  • European Commission - The Role of Lipolysis in the Pathogenesis of Cancer-associated Cachexia [340896]
Citation (ISO format)
BAAZIM, Hatoon et al. CD8+ T cells induce cachexia during chronic viral infection. In: Nature Immunology, 2019, vol. 20, n° 6, p. 701–710. doi: 10.1038/s41590-019-0397-y
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Article (Published version)
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Identifiers
ISSN of the journal1529-2908
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