Lack of immunohistological changes in the islets of nondiabetic, autoimmune, polyendocrine patients with β-selective GAD-specific islet cell antibodies

Richard Wagner, Jessica M. McNally, Ezio Bonifacio, Stefano Genovese, Alan Foulis, Margaret McGill, Michael R. Christie, Corrado Betterle, Emanuele Bosi, Gian Franco Bottazzo

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

We examined the pancreases from three nondiabetic, autoimmune, polyendocrine patients with islet cell antibodies (ICAs) and glutamic acid decarboxylase (GAD) antibodies who died without developing insulin-dependent diabetes mellitus (IDDM). All three patients had the β-selective GAD- specific ICA subtype and antibodies to the GAD-derived 50 kD tryptic fragment. None had whole islet ICA or antibodies to the non-GAD-derived 37k islet antigen, which appear to be more closely associated with IDDM than antibodies to GAD. The three patients also were negative for insulin autoantibodies. Islets within pancreas from patients 1 and 2 appeared well preserved as assessed by hematoxylin and eosin staining. In these two patients, insulin content, as assessed by indirect immunofluorescence on cryostat sections, was normal. Patient 3 had a prolonged postmortem time, and the islet insulin content was reduced slightly. In all three pancreases, no evidence was found of increased human leukocyte antigen class I or de novo class II molecule expression on islet cells, and islet infiltration by T- or B-cells or macrophages was not detected. Islet capillary endothelial cells did not show signs of hypertrophy. No immunoglobulin or complement deposition within or around islets was found. These data indicate that humoral GAD autoimmunity does not necessarily associate with visible β-cell damage.

Original languageEnglish
Pages (from-to)851-856
Number of pages6
JournalDiabetes
Volume43
Issue number7
Publication statusPublished - 1994

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Glutamate Decarboxylase
Pancreas
Antibodies
Insulin
Type 1 Diabetes Mellitus
Carboxy-Lyases
Hematoxylin
Eosine Yellowish-(YS)
Indirect Fluorescent Antibody Technique
HLA Antigens
Autoimmunity
Islets of Langerhans
Autoantibodies
Hypertrophy
islet cell antibody
Immunoglobulins
B-Lymphocytes
Endothelial Cells
Macrophages
Staining and Labeling

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Lack of immunohistological changes in the islets of nondiabetic, autoimmune, polyendocrine patients with β-selective GAD-specific islet cell antibodies. / Wagner, Richard; McNally, Jessica M.; Bonifacio, Ezio; Genovese, Stefano; Foulis, Alan; McGill, Margaret; Christie, Michael R.; Betterle, Corrado; Bosi, Emanuele; Bottazzo, Gian Franco.

In: Diabetes, Vol. 43, No. 7, 1994, p. 851-856.

Research output: Contribution to journalArticle

Wagner, R, McNally, JM, Bonifacio, E, Genovese, S, Foulis, A, McGill, M, Christie, MR, Betterle, C, Bosi, E & Bottazzo, GF 1994, 'Lack of immunohistological changes in the islets of nondiabetic, autoimmune, polyendocrine patients with β-selective GAD-specific islet cell antibodies', Diabetes, vol. 43, no. 7, pp. 851-856.
Wagner, Richard ; McNally, Jessica M. ; Bonifacio, Ezio ; Genovese, Stefano ; Foulis, Alan ; McGill, Margaret ; Christie, Michael R. ; Betterle, Corrado ; Bosi, Emanuele ; Bottazzo, Gian Franco. / Lack of immunohistological changes in the islets of nondiabetic, autoimmune, polyendocrine patients with β-selective GAD-specific islet cell antibodies. In: Diabetes. 1994 ; Vol. 43, No. 7. pp. 851-856.
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abstract = "We examined the pancreases from three nondiabetic, autoimmune, polyendocrine patients with islet cell antibodies (ICAs) and glutamic acid decarboxylase (GAD) antibodies who died without developing insulin-dependent diabetes mellitus (IDDM). All three patients had the β-selective GAD- specific ICA subtype and antibodies to the GAD-derived 50 kD tryptic fragment. None had whole islet ICA or antibodies to the non-GAD-derived 37k islet antigen, which appear to be more closely associated with IDDM than antibodies to GAD. The three patients also were negative for insulin autoantibodies. Islets within pancreas from patients 1 and 2 appeared well preserved as assessed by hematoxylin and eosin staining. In these two patients, insulin content, as assessed by indirect immunofluorescence on cryostat sections, was normal. Patient 3 had a prolonged postmortem time, and the islet insulin content was reduced slightly. In all three pancreases, no evidence was found of increased human leukocyte antigen class I or de novo class II molecule expression on islet cells, and islet infiltration by T- or B-cells or macrophages was not detected. Islet capillary endothelial cells did not show signs of hypertrophy. No immunoglobulin or complement deposition within or around islets was found. These data indicate that humoral GAD autoimmunity does not necessarily associate with visible β-cell damage.",
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T1 - Lack of immunohistological changes in the islets of nondiabetic, autoimmune, polyendocrine patients with β-selective GAD-specific islet cell antibodies

AU - Wagner, Richard

AU - McNally, Jessica M.

AU - Bonifacio, Ezio

AU - Genovese, Stefano

AU - Foulis, Alan

AU - McGill, Margaret

AU - Christie, Michael R.

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AU - Bosi, Emanuele

AU - Bottazzo, Gian Franco

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AB - We examined the pancreases from three nondiabetic, autoimmune, polyendocrine patients with islet cell antibodies (ICAs) and glutamic acid decarboxylase (GAD) antibodies who died without developing insulin-dependent diabetes mellitus (IDDM). All three patients had the β-selective GAD- specific ICA subtype and antibodies to the GAD-derived 50 kD tryptic fragment. None had whole islet ICA or antibodies to the non-GAD-derived 37k islet antigen, which appear to be more closely associated with IDDM than antibodies to GAD. The three patients also were negative for insulin autoantibodies. Islets within pancreas from patients 1 and 2 appeared well preserved as assessed by hematoxylin and eosin staining. In these two patients, insulin content, as assessed by indirect immunofluorescence on cryostat sections, was normal. Patient 3 had a prolonged postmortem time, and the islet insulin content was reduced slightly. In all three pancreases, no evidence was found of increased human leukocyte antigen class I or de novo class II molecule expression on islet cells, and islet infiltration by T- or B-cells or macrophages was not detected. Islet capillary endothelial cells did not show signs of hypertrophy. No immunoglobulin or complement deposition within or around islets was found. These data indicate that humoral GAD autoimmunity does not necessarily associate with visible β-cell damage.

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