Autoimmunity in chronic obstructive pulmonary disease: clinical and experimental evidence

Expert Rev Clin Immunol. 2012 Mar;8(3):285-92. doi: 10.1586/eci.12.7.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Adaptive Immunity
  • Animals
  • Autoimmunity
  • Humans
  • Immunity, Innate
  • Interferon-gamma / immunology
  • Interleukin-17 / immunology
  • Pulmonary Disease, Chronic Obstructive / complications
  • Pulmonary Disease, Chronic Obstructive / immunology*
  • Pulmonary Emphysema / etiology
  • Pulmonary Emphysema / immunology*
  • Smoking / adverse effects
  • Th1 Cells / immunology*
  • Th17 Cells / immunology*


  • Interleukin-17
  • Interferon-gamma