Peripheral T-lymphocytes in Juvenile-onset Diabetics (JOD) and in Maternity-onset Diabetics (MOD)

Cattaneo, R; Saibene, V.; Pozza, G.

doi:10.2337/diab.25.3.223

Cited by 21 publications

(10 citation statements)

References 5 publications

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“…The data presented show a significant reduction of peripheral T-lymphocyte percentage in insulin dependent diabetics. These results agree with previous reports from this laboratory [9,11] and with findings from other authors [10,12,13], but differ from Lymphocyte E-rosetting % Basal (11) 57.9 _+ 3.6 Glucose 100 mg/100ml (11) 51.0 _+ 3.2 NS Glucose 300 mg/100ml (11) 50.5 _+ 3.2 NS Glucose 500 rag/100 ml (10) 51.1 _+ 3.9 NS NS = not significant those of MacCuish et al [14] and Hann et al [22]. The discrepancies may be due both to difference in methods and to heterogeneity among the examined patients.…”

Section: Discussionsupporting

confidence: 94%

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Factors affecting E-rosette forming ability in peripheral lymphocytes of insulin dependent diabetics

Cattaneo

Saibene

et al. 1980

Diabetologia

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Poorly controlled insulin dependent diabetics showed impaired E-rosette forming ability compared to sex and age matched normal controls (34.8 + 3.1, n = 31 vs 55.5 _+ 1.7, n = 33; p < 0.001; mean + SEM). The reduction of E-rosette cells % was not related to the duration of diabetes, nor to fasting blood glucose levels. Incubation of lymphocytes from a subsequent series of 17 insulindependent diabetics with insulin (100 ~tU/ml) plus glucose (100 mg/100 ml) significantly increased Erosette formation (37.6 _+ 3.3 vs 47.0 _+ 2.2; p = 0.01); conversely glucagon (0.1 ~tg/ml) significantly impaired E-rosette forming ability of normal lymphocytes (51.5 + 3.6 vs 44.5 + 4.2; n-17; p < 0.01). No difference was observed in cAMP content of normal and diabetic lymphocytes, nor was Erosette forming ability related to intracellular cAMP content. Incubation with increasing glucose concentrations (up to 500mg/100ml) did not affect Erosette forming ability of normal lymphocytes. Incubation of normal lymphocytes with diluted (1:10) serum from sex and age matched insulin dependent diabetics impaired E-rosette forming ability to the level found in diabetics (61.1 + 2.9 vs 39.7 _+ 4.4; p < 0.001). The results of these in vitro experiments show that insulin and glucagon exhibit opposite effects on E-rosette forming ability and that undefined factor(s) present in diabetic serum may affect this T-cell function.

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Section: Discussionsupporting

confidence: 94%

“…As to cell mediated immunity, there are reports of T-cell defects, manifested by low counts of Erosette forming cells [9,10,11,12,13] and impaired in vitro response to T-cell mitogens [14,15].…”

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confidence: 99%

Factors affecting E-rosette forming ability in peripheral lymphocytes of insulin dependent diabetics

Cattaneo

Saibene

et al. 1980

Diabetologia

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“…Cell-mediated immunity like heredity, virus infections [1] and humoral immunity [2] may play an important role in the aetiology of diabetes [3][4][5][6]. Studies on circulating lymphocytes in diabetics have given variable results [7][8][9][10][11][12][13] which may be due to differences in methodology, selection of patients or metabolic control at the time of the study. In order to re-examine these findings, we have studied circulating lymphocyte subpopulations in the juvenile insulin dependent type of diabetes which may be related aetiologically to immunological factors [14,15].…”

mentioning

confidence: 99%

Circulating lymphocyte subpopulations in juvenile insulin-dependent diabetes

et al. 1979

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Circulating lymphocytes from 39 juvenile insulin dependent diabetics of recent onset were studied by six membrane marker techniques and mitogen stimulation. Well controlled (n = 14) were grouped separately from poorly controlled (n = 25) patients. The total lymphocyte counts were not different from 50 control subjects. The percentage of T-cells detected by erythrocyte rosettes and B-cells detected by erythrocytes--antibody--complement rosettes was significantly decreased only in poorly-controlled diabetics (64.1 +/- 1.3 and 9.7 +/- 1.8, vs 71.0 +/- 1.0 and 15.3 +/- 0.6 in controls). Cells bearing receptors for the Fc fragment of IgG immunoglobulins were decreased in both groups. Mitogen stimulation was not different from controls but was significantly lower in poorly controlled than in well controlled diabetics. Optimal blood glucose control for 5 +/- 2 days using an external artificial pancreas led to a rapid normalisation of membrane marker values and mitogen responsiveness of lymphocytes from previously poorly controlled diabetics. Separate in vitro experiments showed that glucose had an inhibitory effect on mitogen stimulation at concentrations greater than or equal to 8.3 mmol/l and on T- and B-lymphocyte numbers at concentrations greater than or equal to 55.6 mmol/l. DL 3-hydroxybutyrate tested at 17.1 and 34.2 mmol/l only depressed mitogen responsiveness. Such results suggest a rapidly reversible T-cell defect closely linked to the existing metabolic disturbances.

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“…An alternate possibility is that a virus might produce a low-grade persistent or non-lyric infection of beta, cells ~nd that destruction of the infected beta cells is due to the immune response of the host. Others demonstrated that antigens from pancreatic tissue inhibited to a markedly greater extent the migration of leukocytes from insulin-dependent diabetics than from controls (46, 57--59, 69) and in one study, it ws~s reported that the percentage of peripheral T lymphoeytes was decreased in patients with juvenile-onset as compared to maturity-onset diabetes (9). Recently, however, investigators from several laboratories found that diabetic patients respond immunologically to pancreatic tissue.…”

Section: Genetic and Immunologic Factorsmentioning

confidence: 99%