Abstract
NK and NKT-like cells represent a small but important proportion of effector lymphocytes that we have previously shown to be a major source of pro-inflammatory cytokines and granzymes1. We hypothesized that NK and NKT-like cells would be increased in the airway in COPD and that this would be accompanied by a reduction in expression of the inhibitory receptor CD94 (Kp43) and increased expression of the cytotoxic mediators granzyme B and perforin.
We measured NK and NK-like T-cells and their expression of CD94 in the blood of patients with COPD (n=61), smokers (16) and healthy controls (25) and BAL from a cohort of subjects. We further assessed activation by expression of CD69 and cytotoxic potential by production of granzymes A and B and using a cytotoxicity assay.
In blood from COPD subjects, there were no significant changes in NK or NKT-like cell numbers or expression of granzyme A or cytotoxic potential vs controls. There was however, increased expression of granzyme B and decreased expression of CD94 by both cell types vs controls.
In the airway in COPD, NK and NKT-like numbers were increased, associated with increased NK cytotoxicity, increased expression of granzyme B and decreased expression of the inhibitory receptor CD94.
Treatment strategies that target NK and NKT-like cells, their cytotoxicity and production of inflammatory mediators in the airway may improve COPD morbidity.
- © 2012 ERS