T-cell growth factor (TCGF) activity was studied in phytohaemoagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMC) from 10 type-1 diabetic patients who had been diagnosed within the previous 12 months (group A), from 9 diabetic patients in whom the duration of disease was more than 1 year (group B) and from 12 healthy controls (group C). The effects of indomethacin on PHA-induced TCGF activity and the effects of adherent cells (macrophages) from group A and group C on TCGF production of normal group-matched non-adherent cells (lymphocytes) were also studied. TCGF activity was assayed on TCGF-dependent blast cells and calculated as a stimulation index (SI). TCGF activity in group A (SI 0.86±0.8) was significantly different from that in group B (SI 1.75±1.02;P=0.037) and in group C (SI 1.91±1.29;P=0.023). Following the addition of indomethacin, TCGF SI was 1.35±0.74 in group A, 1.85±0.73 in group B and 2.06±1.19 in group C. The responses to indomethacin were found to correlate with the basal TCGF activity in all subjects (r=-0.48;P=0.006) independently of the disease process studied or its duration. No correlation was found between TCGF activity and parameters of metabolic control (HBA1c and fructosamine). Interestingly, a significant inverse correlation was found between TCGF activity and the required dose of insulin only in group A (r=-0.66;P<0.05). Adherent cells from diabetic patients were found not to inhibit TCGF production. Our results suggest that a defect in T-cell growth-promoting lymphokines could be a relevant feature of type-1 diabetes mellitus in the first months following clinical diagnosis and possibly the lack of detection of this defect in long-standing diabetes may be evidence of ongoing beta cell mass destruction. This defect does not appear to be related to an inhibitory effect mediated by adherent cells or prostaglandins. © 1994 Springer-Verlag.
Impairment of T-cell growth-promoting lymphokines in human insulin-dependent diabetes mellitus
Badolato R.;
1994-01-01
Abstract
T-cell growth factor (TCGF) activity was studied in phytohaemoagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMC) from 10 type-1 diabetic patients who had been diagnosed within the previous 12 months (group A), from 9 diabetic patients in whom the duration of disease was more than 1 year (group B) and from 12 healthy controls (group C). The effects of indomethacin on PHA-induced TCGF activity and the effects of adherent cells (macrophages) from group A and group C on TCGF production of normal group-matched non-adherent cells (lymphocytes) were also studied. TCGF activity was assayed on TCGF-dependent blast cells and calculated as a stimulation index (SI). TCGF activity in group A (SI 0.86±0.8) was significantly different from that in group B (SI 1.75±1.02;P=0.037) and in group C (SI 1.91±1.29;P=0.023). Following the addition of indomethacin, TCGF SI was 1.35±0.74 in group A, 1.85±0.73 in group B and 2.06±1.19 in group C. The responses to indomethacin were found to correlate with the basal TCGF activity in all subjects (r=-0.48;P=0.006) independently of the disease process studied or its duration. No correlation was found between TCGF activity and parameters of metabolic control (HBA1c and fructosamine). Interestingly, a significant inverse correlation was found between TCGF activity and the required dose of insulin only in group A (r=-0.66;P<0.05). Adherent cells from diabetic patients were found not to inhibit TCGF production. Our results suggest that a defect in T-cell growth-promoting lymphokines could be a relevant feature of type-1 diabetes mellitus in the first months following clinical diagnosis and possibly the lack of detection of this defect in long-standing diabetes may be evidence of ongoing beta cell mass destruction. This defect does not appear to be related to an inhibitory effect mediated by adherent cells or prostaglandins. © 1994 Springer-Verlag.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
