Autoimmunity in chronic obstructive pulmonary disease: clinical and experimental evidence

Abstract

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.

Keywords::

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

Acknowledgements

The authors thank the Corry/Kheradmand laboratory members for their insightful comments.

Financial & competing interests disclosure

Funding from the NIH (HL072419-A1) and Veterans Administration Medical Center paid part of F Kheradmand’s salary and postdoctoral research to study the role of T cells in human COPD and emphysema. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.