ISSN:
1432-5233
Keywords:
Insulin dependent diabetes mellitus
;
T-cell growth factor
;
T lymphocytes
;
Macrophages
;
Indomethacin
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00580762
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