In vitro secretion of interleukin-1 beta and interferon-gamma by peripheral blood lymphomononuclear cells in diabetic patients.
Diabetes Res Clin Pract
; 21(2-3): 87-93, 1993.
Article
em En
| MEDLINE
| ID: mdl-8269823
ABSTRACT
There is evidence that cytokines, in particular interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma) might mediate beta cell destruction in type 1 diabetes. Therefore the secretion of these cytokines by peripheral blood lymphomononuclear cells (PBMNC) was investigated in basal conditions and 48 h after stimulation with T-cell mitogen phytohaemagglutinin (PHA) in 33 diabetic patients and in 10 normal controls. The patients were divided in 4 groups (Group 1, 10 controls; Group 2, 13 newly diagnosed type 1 diabetics, the onset had occurred from 5 days to 3 months before the study; Group 3, 10 Long Standing (LS) type 1 diabetics with duration of the disease between 2 years and 10 years; and Group 4, 10 type 2 diabetics). No difference was found among the 4 groups considered in IL-1 beta secretion by unstimulated cultures, although the percentage of TAC+ cells was significantly higher in type 1 newly diagnosed diabetic patients with respect to the LS, the type 2 diabetics and the controls. After PHA stimulation a significant increase of IL-1 beta was found in newly diagnosed type 1 diabetic patients in comparison with the control subjects, the LS and type 2 diabetic patients (P < 0.001). The supernatants of newly diagnosed type 1 diabetics also showed a significant reduction in IFN-gamma production both in basal (P < 0.01) and in stimulated conditions (P < 0.001) in comparison with the controls, the LS (P < 0.002 in basal, and P < 0.001 in stimulated conditions) and the type 2 diabetic patients (P < 0.001 both in basal and stimulated conditions).(ABSTRACT TRUNCATED AT 250 WORDS)
Buscar no Google
Base de dados:
MEDLINE
Assunto principal:
Linfócitos
/
Linfócitos T
/
Interferon gama
/
Interleucina-1
/
Diabetes Mellitus Tipo 1
/
Diabetes Mellitus Tipo 2
Idioma:
En
Ano de publicação:
1993
Tipo de documento:
Article