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Tissue-resident CD8+ T cells drive age-associated chronic lung sequelae after viral pneumonia

Nick P Goplen1,2, Yue Wu3, Young Min Son1

  • 1Division of Pulmonary and Critical Medicine, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA.

Science Immunology
|November 7, 2020
PubMed

Insights

Aging impairs CD8+ T cells, causing chronic lung inflammation after viral pneumonia. Depleting these dysfunctional T cells resolves inflammation and fibrosis in older animals, highlighting age-related immune deficits.

Area of Science:

  • Immunology
  • Gerontology
  • Respiratory Medicine

Background:

  • Lower respiratory viral infections, including influenza and SARS-CoV-2, cause severe pneumonia in the elderly.
  • Aging is associated with altered immune responses and increased susceptibility to infections.

Purpose of the Study:

  • To investigate the role of CD8+ tissue-resident memory T cells (T_RM) in chronic lung pathology following viral pneumonia in aged individuals.
  • To understand the mechanisms underlying T_RM dysfunction and its contribution to persistent inflammation and fibrosis.

Main Methods:

  • Induction of influenza viral pneumonia in aged and young animal models.
  • Analysis of CD8+ T_RM cell accumulation, phenotype, and function in aged lungs.
  • Assessment of the impact of CD8+ T_RM cell depletion on lung inflammation and fibrosis.

Main Results:

  • Influenza viral pneumonia in aged hosts leads to nonresolving lung pathology and increased CD8+ T_RM cell accumulation.
  • Age-associated T_RM cells exhibit impaired TCR signaling and effector functions, linked to elevated TGF-β.
  • Depletion of CD8+ T_RM cells reduces chronic inflammation and fibrosis in aged animals.

Conclusions:

  • Age-associated malfunction of CD8+ T_RM cells exacerbates chronic lung inflammation and fibrosis post-viral pneumonia.
  • Targeting these dysfunctional T cells may offer therapeutic strategies for age-related respiratory complications.

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