• Corry-Anke Brandsma, Huib A M Kerstjens, Wouter H van Geffen, Marie Geerlings, Dirkje S Postma, Machteld N Hylkema, and Wim Timens.
• Dept of Pathology and Medical Biology, University Medical Center Groningen and University of Groningen, P.O. box 30.001, 9700 RB, Groningen, The Netherlands. c.a.brandsma@umcg.nl
• Eur. Respir. J. 2012 Aug 1; 40 (2): 313-21.

AbstractSeveral studies have demonstrated the presence of B-cell follicles and autoantibodies in chronic obstructive pulmonary disease (COPD). It is unclear against which antigens this B-cell response is directed and whether it contributes to development or worsening of disease. We assessed different B-cell subsets in blood and lung tissue from COPD patients and controls, and compared differences in B-cell responsiveness to stimulation with lung-specific antigens. Active smoking induced an adaptive immune response with relatively high levels of (class-switched) memory B-cells in blood and immunoglobulin (Ig)G memory B-cells in the lung. COPD smokers showed more switching to IgG, whereas healthy smokers switched more to IgA. COPD patients had higher levels of memory B-cells in the lung and stimulation with lung-specific antigens induced higher numbers of anti-decorin antibody-producing cells in COPD patients compared with healthy controls. Differential switching to IgG and IgA indicates that the adaptive immune response to smoke differs between COPD patients and healthy controls. A higher level of memory B-cells in the lungs of COPD patients may reflect an antigen-specific immune response, which could be directed against decorin, as suggested by the induction of anti-decorin antibody-producing cells in response to antigen-specific stimulation in COPD patients.

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