Kraft, M. (Monica)
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- B cell–adaptive immune profile in emphysema-predominant chronic obstructive pulmonary disease(American Thoracic Society, 2019) Martinez, F.D. (Fernando D.); Bastarrika, G. (Gorka); Kraft, M. (Monica); Bagevalu, B. (Bhavani); Glass, C. (Carolyn); Polverino, F. (Francesca); San-José-Estépar, R. (Raúl); Torres, J.P. (Juan P.) de; Sullivan, J.L. (John Lawrence); Guerra, S. (Stefano); Sholl, L. (Lynette)Cigarette smoke, the major risk factor for COPD in developed countries, causes pulmonary inflammation that persists long after smoking cessation, suggesting self-perpetuating adaptive immune responses similar to those that occur in autoimmune diseases. Increases in the number and size of B cell–rich lymphoid follicles (LFs) have been shown in patients in severe stages of COPD (4), and increased B-cell products (autoantibodies) have been observed in the blood and lungs of patients with COPD (5, 6). Oligoclonal rearrangement of the immunoglobulin genes has been observed in B cells isolated from COPD LFs, suggesting that a specific antigenic stimulation drives B-cell proliferation. Consistently, we have shown that in the COPD lung, there is an overexpression of BAFF (B-cell activation factor of the TNF family), which is a key regulator of B-cell homeostasis in several autoimmune diseases (7) and is involved in the growth of LFs in COPD. However, a network analysis of lung transcriptomics showed that a prominent B-cell molecular signature characterized emphysema preferentially but was absent in AD independently of the degree of airflow limitation (8). In the current study, we investigated the correlation between B-cell responses in lung tissue from patients with COPD and healthy smokers, and the extent of emphysema versus airflow limitation.