Recent evidence indicates that activation of adaptive immunity in COPD per- sists after smoking cessation, suggesting self-perpetuating mechanisms similar to those occurring in autoimmune diseases. Antielastin and antiepithelial au- toantibodies have been detected in COPD indicating that B cells contribute to development of the disease. B cell Activating Factor of TNF Family (BAFF) is a crucial factor that modulates B cell-tolerance and homeostasis and its upregulation promotes autoimmune responses. BAFF expression was quantified by immuno- histochemistry in lung specimens from 21 smokers with COPD (GOLD I-IV, FEV1=57±25%pred); 14 control smokers (FEV1=100±9%pred) and 8 nonsmok- ers (FEV1=104±10%pred) undergoing surgery for pulmonary nodule or LVRS. BAFF was quantified in alveolar macrophages, in parenchymal and bronchiolar lymphoid follicles. COPD patients had higher BAFF expression in alveolar macro- phages (Median;Range: 64;2-95%) when compared to smoking (36;4-70%;p=0.04) and nonsmoking controls (20;0-54%; p=0.003). In parenchymal lymphoid follicles, BAFF expression was increased in COPD (2;0-8 foll/cm2) compared to smoking (1;0-6 foll/cm2 ;p=0.04) and nonsmoking controls (0;0-2 foll/cm2 ;p=0.002). The analysis of lymphocyte composition of BAFF+ follicles revealed that the great majority was composed of B lymphocytes. The percentage of airways with BAFF+ follicles was also increased in COPD patients (17;0-100%) as compared to non smoking controls (0;0-0%;p=0.01). In conclusion, BAFF expression is increased in alveolar macrophages and lymphoid follicles of patients with COPD. These results support the view that B lymphocyte expansion, mediated by BAFF, is a critical event in the pathogenesis of COPD.
Overexpression of B cell activating factor (BAFF) in peripheral lung of COPD patients
PAPI, Alberto;
2009
Abstract
Recent evidence indicates that activation of adaptive immunity in COPD per- sists after smoking cessation, suggesting self-perpetuating mechanisms similar to those occurring in autoimmune diseases. Antielastin and antiepithelial au- toantibodies have been detected in COPD indicating that B cells contribute to development of the disease. B cell Activating Factor of TNF Family (BAFF) is a crucial factor that modulates B cell-tolerance and homeostasis and its upregulation promotes autoimmune responses. BAFF expression was quantified by immuno- histochemistry in lung specimens from 21 smokers with COPD (GOLD I-IV, FEV1=57±25%pred); 14 control smokers (FEV1=100±9%pred) and 8 nonsmok- ers (FEV1=104±10%pred) undergoing surgery for pulmonary nodule or LVRS. BAFF was quantified in alveolar macrophages, in parenchymal and bronchiolar lymphoid follicles. COPD patients had higher BAFF expression in alveolar macro- phages (Median;Range: 64;2-95%) when compared to smoking (36;4-70%;p=0.04) and nonsmoking controls (20;0-54%; p=0.003). In parenchymal lymphoid follicles, BAFF expression was increased in COPD (2;0-8 foll/cm2) compared to smoking (1;0-6 foll/cm2 ;p=0.04) and nonsmoking controls (0;0-2 foll/cm2 ;p=0.002). The analysis of lymphocyte composition of BAFF+ follicles revealed that the great majority was composed of B lymphocytes. The percentage of airways with BAFF+ follicles was also increased in COPD patients (17;0-100%) as compared to non smoking controls (0;0-0%;p=0.01). In conclusion, BAFF expression is increased in alveolar macrophages and lymphoid follicles of patients with COPD. These results support the view that B lymphocyte expansion, mediated by BAFF, is a critical event in the pathogenesis of COPD.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
