Autoimmunity in chronic obstructive pulmonary disease: Clinical and experimental evidence

Farrah Kheradmand, Ming Shan, Chuang Xu, David Corry

Research output: Contribution to journalReview articlepeer-review

73 Scopus citations


Over the past few decades, neutrophils and macrophages had co-occupied center stage as the critical innate immune cells underlying the pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease and lung parenchymal destruction (i.e., emphysema). While chronic exposure to smoke facilitates the recruitment of innate immune cells into the lung, a clear role for adaptive immunity in emphysema has emerged. Evidence from human studies specifically point to a role for recruitment and activation of pathogenic lymphocytes and lung antigen-presenting cells in emphysema; similarly, animal models have confirmed a significant role for autoimumnity in progressive smoke-induced emphysema. Increased numbers of activated antigen-presenting cells, Th1 and Th17 cells, have been associated with smoke-induced lung inflammation and production of the canonical cytokines of these cells, IFN-γ and IL-17, correlates with disease severity. These exciting new breakthroughs could open new avenues for developing effective new therapies for smoke-induced emphysema.

Original languageEnglish (US)
Pages (from-to)285-292
Number of pages8
JournalExpert Review of Clinical Immunology
Issue number3
StatePublished - Mar 2012


  • adaptive immunity
  • antigen-presenting cells
  • cytokines
  • Th1
  • Th17

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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