ISSN:
1432-0428
Schlagwort(e):
Key words Bcl-2
;
apoptosis
;
T cells
;
flow cytometry
;
cell-mediated immunity in insulin-dependent diabetes mellitus.
Quelle:
Springer Online Journal Archives 1860-2000
Thema:
Medizin
Notizen:
Summary The bcl-2 gene product has been shown to regulate apoptotic cell death, and its dysregulation has been shown to induce several abnormalities in the immune system. No data exist regarding bcl-2 expression in autoimmune diseases, such as human insulin-dependent diabetes mellitus (IDDM). We investigated bcl-2 protein expression by testing T lymphocytes from 15 newly-diagnosed ( 〈 3 weeks) IDDM patients in comparison to 10 age-matched control subjects. The expression of bcl-2 on CD3 + lymphocyte subsets was investigated after membrane permeabilization by two- or three-colour immunofluorescence. When the percentage and mean fluorescence intensity (MFI) of bcl-2 + /CD3 + cells from normal individuals and patients were compared, we found that bcl-2 expression within the CD3 + and CD4 + CD45R0 + T-cell populations was reduced significantly in IDDM patients (46.8 ± 15.4 vs 79.6 ± 11.7; 25.7 ± 3.8 vs 47.15 ± 5.7, respectively; p 〈 0.001). To establish whether low bcl-2 expression in T cells from newly-diagnosed patients reflects their susceptibility to death by an apoptotic process, we also evaluated DNA staining with propidium iodide in CD3 + lymphocyte suspension after a (24–72 h) culture period (spontaneous apoptosis). We found that IDDM patients have higher levels of spontaneous apoptosis (mean ± SEM: 24 h = 4.6 ± 0.8; 48 h = 9.9 ± 1; 72 h = 12.8 ± 1.1) than control subjects (24 h = 1.8 ± 0.4; 48 h = 4.6 ± 0.4; 72 h = 5.7 ± 0.3; p 〈 0.02–0.001). Our study suggests that recent onset IDDM is characterised by reduced bcl-2 expression, which in turn may be associated with the increased spontaneous apoptosis we observed. [Diabetologia (1995) 38: 953–958]
Materialart:
Digitale Medien
URL:
http://dx.doi.org/10.1007/BF00400585
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