engleski

Expression of CD38 and its ligand CD31 on normal and in interstitial lung diseases (IDL) BAL cells

CD38 cell surface molecule is considered as a marker of immune activation and/or is involved in the regulation of lymphocyte adhesion endothelial cells. However, in vivo functgion of CD38 in lungs remains unclear, mainly due to the lack of evidence concerning its ligand repertoire. Recent data show that CD38+ cells interact with the ligand CD31 on vascular endothel, where CD38-CD31 molecules behave in a selectin-like manner, promoting the rolling of lymphocytes over the endothelial layer. CD38 molecule may promote cell recruitment in bronchoalveolar space and drive from peripheral blood. Therefore we wanted to drqw information on the biological relevance of CD38-CD38L system in lung interstitium. We analysed BAL profiles of 42 patients: with active sarcoidosis (AS=19), inactive sarcoidosis (IS=15) and fibrosis (F=9) and compared the data with the same parameters in 9 healthy volunteers (C). Three color flow cytometry was used to examine the surface expression of CD38 (B. Dickinson) and CD31 (Moon-1, F. Malavasi) phenotype of CD4, CD8 and HLA-DR lymphocytes (L), macrophages (M), granulocytes (G) in BAL. The results are wxpressed as mean percentages of CD38+ and CD31+ subpopulations. In healthy individuals CD38 was evident on L (7%) and in the trace on M and G, whereas CD31 was found mostly on M (22%), and in a lower extent on L and G (12 and 10%). Also both CD4 and CD8 subsets bearing CD38 and HLA-DR were low, whereas in ILD they demonstrate evidence of recent activation. In ILD CD38+ and CD31+ cells were elevated in comparison to C. The highest percentages of CD38+ and CD31+ BAL cells were detected in patients with AS (46 and 21%). In the differential BAL subsets analysis in one patients with AS we present a dramatic and progressive increase of CD38+ (L=88%, M=70%, G=35%) and CD31 (20%, 45% and 90%, respectively). our preliminary results indicate that both CD38 and its ligand CD31 in BAL, could serve as local regulatory molecules, whose main effect probably encompasses many other organic systems. Whether CD38+ and CD31+ cells are involved in inducing inflammation, or have become active as a result of migration through the endothelium, remains to be determined.

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