Islet-Cell Antibodies in Diabetes Mellitus With Autoimmune Polyendocrine Deficiencies

Bottazzo, G. F.; Florin-Christensen, A; Doniach, Deborah

doi:10.1016/s0140-6736(74)90140-8

Cited by 1,338 publications

(632 citation statements)

References 16 publications

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“…ICA were determined by an indirect immunofluoresence technique on unfixed cryostat sections of blood group 0 pancreas [1].…”

Section: Laboratory Methodsmentioning

confidence: 99%

“…The appearance of Type i diabetes is accompanied by multiple circulating autoantibodies: islet cell antibodies (ICA), islet cell surface antibodies (ICSA), insulin autoantibodies (IAA) and anti-64 kilodalton (kd) antibodies. Some of these autoantibodies are observed in 50-90% of newly diagnosed Type i diabetes patients and in 30-50% of their first degree relatives [1][2][3][4][5]. There is accumulating evidence which supports the importance of T-cell mediated autoimmunity in the initiating events of the islet Beta-cell destruction [6][7][8].…”

mentioning

confidence: 99%

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Elevated serum placental isoferritin in newly diagnosed Type 1 (insulin-dependent) diabetes mellitus. A possible marker for identification of high risk subjects

Assa¹,

Moroz

1990

Diabetologia

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“…ICA were determined by an indirect immunofluoresence technique on unfixed cryostat sections of blood group 0 pancreas [1].…”

Section: Laboratory Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Elevated serum placental isoferritin in newly diagnosed Type 1 (insulin-dependent) diabetes mellitus. A possible marker for identification of high risk subjects

Assa¹,

Moroz

1990

Diabetologia

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“…Whether this damage occurs by autoimmune mechanisms, as in Type I (insulin-dependent) diabetes mellitus [1], or by other less defined phenomena (e.g., glucose toxicity [2], lipotoxicity [3], prolonged excessive insulin secretion [4]), as in Type II (non-insulin-dependent) diabetes mellitus [5], the final result is impaired insulin secretion [6]. A number of autoantibodies (aAbs) marking the immune-mediated destruction of the beta cell typical of Type I diabetes have been described since the identification of islet cell antibodies (ICA) [7]. ICA comprise a number of autoreactive immunoglobulins with different target antigens, one of which has later been identified as GAD [8,9].…”

mentioning

confidence: 99%

Anti-CD38 autoantibodies: Characterisation in new-onset Type I diabetes and latent autoimmune diabetes of the adult (LADA) and comparison with other islet autoantibodies

Mallone¹,

Ortolan²,

Pinach³

et al. 2002

Diabetologia

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Aims/hypothesis. Serum anti-CD38 autoantibodies (aAbs) have been reported in 17 to 19% of patients with long-standing Type I (insulin-dependent) diabetes mellitus and Type II (non-insulin-dependent) diabetes mellitus. Whether these aAbs are also found in new-onset Type I diabetes and in Latent Autoimmune Diabetes in Adults (LADA) is not known, as is their relationship with conventional islet aAbs. Methods. These issues were addressed by studying new-onset Type I and LADA diabetic cohorts with a recently developed anti-CD38 enzymatic immunoassay. Results. Anti-CD38 aAb prevalence among newonset Type I patients (3.8%) was lower than previously found in long-standing Type I diabetes (11.7%, as defined with the 97.5 percentile cutoff; p=0.01), suggesting a late appearance of these aAbs. Among LADA patients, 14.9% were anti-CD38 + . Anti-CD38 were only associated with anti-GAD aAbs in newonset Type I diabetes. Although the CD38 target molecule was expressed in human pancreatic islets, anti-CD38 aAbs did not contribute to the islet cell antibody (ICA) immunofluorescence reactivity. All the positive sera analysed for Ca 2+ release were found to mobilise it. In agreement with these agonistic features, anti-CD38 + new-onset Type I patients showed higher fasting C-peptide values as compared to negative counterparts; the association was stronger when the analysis was limited to the agonistic anti-CD38 + sera. A similar trend was found among LADA patients. Conclusion/interpretation. Anti-CD38 aAbs are distinct markers of islet autoimmunity which are more prevalent in long-standing disease, as opposed to the other known islet aAbs. Their in vitro agonistic properties could be operating in vivo as well, as they identify sub-groups of patients with higher residual betacell function. [Diabetologia (2002[Diabetologia ( ) 45:1667[Diabetologia ( -1677

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“…In contrast, if the cells were cultured in tissue culture medium 199 supplemented with glucose (5.5 or 16.7retool/I) and 10% heat-inactivated fetal calf serum without 3-isobutyl-l-methylxanthine, cap formation was not detectable. These results suggest that mobile antigen on the surface of pancreatic B cells can be induced to aggregate into patch and cap formations during conditions of increased cellular metabolism.Key words: Rat, islet cell surface antigen, immunobeads, patch and cap formation.The possibility that immunological reactions may be involved in the pathogenesis of insulin-dependent diabetes has been supported by the demonstration of islet cell cytoplasmic antibodies [1,2] and islet cell surface antibodies (ICSA) [3] in the sera from insulin-dependent diabetic patients. Cytoplasmic islet cell antibodies and ICSA are most prevalent at the onset of the disease and decrease thereafter [4].…”

mentioning

confidence: 99%

“…The possibility that immunological reactions may be involved in the pathogenesis of insulin-dependent diabetes has been supported by the demonstration of islet cell cytoplasmic antibodies [1,2] and islet cell surface antibodies (ICSA) [3] in the sera from insulin-dependent diabetic patients. Cytoplasmic islet cell antibodies and ICSA are most prevalent at the onset of the disease and decrease thereafter [4].…”

mentioning

confidence: 99%

Distribution and redistribution of pancreatic islet cell surface antigen reactive with islet cell surface antibody in the rat

Ohgawara

Okano

Kataoka³

et al. 1983

Diabetologia

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Summary. Antigens on the rat pancreatic islet cell surface were redistributed into patch and cap formation when the cells were incubated in the presence of the phosphodiesterase inhibitor, 3-isobutyl-l-methylxanthine, in tissue culture medium 199 for 24 h, before addition of rat pancreatic islet cell surface antibody. In contrast, if the cells were cultured in tissue culture medium 199 supplemented with glucose (5.5 or 16.7retool/I) and 10% heat-inactivated fetal calf serum without 3-isobutyl-l-methylxanthine, cap formation was not detectable. These results suggest that mobile antigen on the surface of pancreatic B cells can be induced to aggregate into patch and cap formations during conditions of increased cellular metabolism.Key words: Rat, islet cell surface antigen, immunobeads, patch and cap formation.The possibility that immunological reactions may be involved in the pathogenesis of insulin-dependent diabetes has been supported by the demonstration of islet cell cytoplasmic antibodies [1,2] and islet cell surface antibodies (ICSA) [3] in the sera from insulin-dependent diabetic patients. Cytoplasmic islet cell antibodies and ICSA are most prevalent at the onset of the disease and decrease thereafter [4]. The role of these antibodies in the pathogenesis of diabetes and the nature of the antigens are still unknown.Scanning electron microscopy has proved to be a useful technique for studying cell surface architecture and has gained wide application in cell biology. The surface architecture of the islet cell was found to change showing an increased number of villi or blebs after incubation in the presence of a high concentration of glu-The present investigation was designed to study the binding of antibodies to rat pancreatic islet cell surface antigen and the effect of the phosphodiesterase inhibitor, 3-isobutyl-l-methylxanthine (IBMX) on the distribution of antigen using scanning electron microscopy and visualizing bound antibodies with immunobeads or indirect immunofluorescence. Materials and Methods Preparation of Dispersed Islet CellsAdult rat pancreatic islets were prepared under sterile conditions by collagenase digestion of the pancreas [6]. Islets were separated from the digests by discontinuous Ficoll gradient centrifugation, and washed by repeated low speed centrifugation in tissue culture medium 199 (TCM 199), before being selected individually by micropipette. The islets were placed in TCM 199 (10 ml) with IBMX (0.1 retool/l), collagenase (30mg), hyarulonidase (20 mg) and ethyleneglycol-bis-(flaminoethyl ether) N, N'-tetra acetic acid (1.0 mmol/1) for 30 rain at 37 ~ in an atmosphere of 5% CO2 and 95% air. The islet suspensions were then kept for 24 h in plastic petri dishes containing TCM 199, further supplemented with 10% heat-inactivated fetal calf serum, penicillin (400 U/ml), glucose (5.5 mmol/1) and IBMX (0.1 mmol/1) [7]. Finally, after resuspension in TCM 199 the islets were disrupted into free cells by mechanical shaking. The dispersed cells were washed by centrifugation in Krebs-Ringer-H...

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Islet-Cell Antibodies in Diabetes Mellitus With Autoimmune Polyendocrine Deficiencies

Cited by 1,338 publications

References 16 publications

Elevated serum placental isoferritin in newly diagnosed Type 1 (insulin-dependent) diabetes mellitus. A possible marker for identification of high risk subjects

Elevated serum placental isoferritin in newly diagnosed Type 1 (insulin-dependent) diabetes mellitus. A possible marker for identification of high risk subjects

Anti-CD38 autoantibodies: Characterisation in new-onset Type I diabetes and latent autoimmune diabetes of the adult (LADA) and comparison with other islet autoantibodies

Distribution and redistribution of pancreatic islet cell surface antigen reactive with islet cell surface antibody in the rat

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