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Tytuł pozycji:

T-cell mediated autoimmunity to the insulinoma-associated protein 2 islet tyrosine phosphatase in type 1 diabetes mellitus.

Tytuł:
T-cell mediated autoimmunity to the insulinoma-associated protein 2 islet tyrosine phosphatase in type 1 diabetes mellitus.
Autorzy:
Dotta F; Department of Endocrinology, University 'La Sapienza', Rome, Italy.
Dionisi S
Viglietta V
Tiberti C
Matteoli MC
Cervoni M
Bizzarri C
Marietti G
Testi M
Multari G
Lucentini L
Di Mario U
Źródło:
European journal of endocrinology [Eur J Endocrinol] 1999 Sep; Vol. 141 (3), pp. 272-8.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: 2023- : Oxford : Oxford University Press
Original Publication: Oslo, Norway : Scandinavian University Press, c1994-
MeSH Terms:
Autoantigens/*immunology
Autoimmunity/*immunology
Diabetes Mellitus, Type 1/*immunology
Membrane Proteins/*immunology
Protein Tyrosine Phosphatases/*immunology
T-Lymphocytes/*immunology
Adolescent ; Adult ; Child ; Child, Preschool ; Electrophoresis, Agar Gel ; Female ; Glutamate Decarboxylase/immunology ; HLA-DR Antigens/analysis ; Histocompatibility Testing ; Humans ; Insulin/immunology ; Male ; Polymerase Chain Reaction ; Protein Tyrosine Phosphatase, Non-Receptor Type 1 ; Radioimmunoassay ; Receptor-Like Protein Tyrosine Phosphatases, Class 8 ; Recombinant Proteins ; Scintillation Counting
Substance Nomenclature:
0 (Autoantigens)
0 (HLA-DR Antigens)
0 (Insulin)
0 (Membrane Proteins)
0 (Recombinant Proteins)
EC 3.1.3.48 (PTPRN protein, human)
EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 1)
EC 3.1.3.48 (Protein Tyrosine Phosphatases)
EC 3.1.3.48 (Ptprn protein, mouse)
EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 8)
EC 4.1.1.15 (Glutamate Decarboxylase)
Entry Date(s):
Date Created: 19990904 Date Completed: 19991112 Latest Revision: 20190905
Update Code:
20231215
DOI:
10.1530/eje.0.1410272
PMID:
10474125
Czasopismo naukowe
The target molecules of the T-cell response in type 1 diabetes, despite their pathogenic importance, remain largely uncharacterized, especially in humans. Interestingly, molecules such as insulin and glutamic acid decarboxylase (GAD) have been shown to be a target not only of autoantibodies, but also of autoreactive T-lymphocytes both in man and in the non-obese diabetic (NOD) mouse. In the present study we aimed to determine the existence of a specific T-cell response towards the insulinoma-associated protein 2 (IA-2) islet tyrosine phosphatase, a recently identified autoantigen which is the target of autoantibodies strongly associated with diabetes development. Human recombinant IA-2 produced in Escherichia coli, was tested for its reactivity with peripheral blood lymphocytes obtained from 16 newly diagnosed type 1 diabetic patients and from 25 normal controls, 15 of whom were HLA-DR-matched. A T-cell proliferation assay was performed in triplicate employing freshly isolated cells in the absence or in the presence of the antigen to be tested (at two different concentrations: 2 microg/ml and 10 microg/ml). A specific T-cell proliferation (defined as a stimulation index (S.I.) >/=3) was observed against IA-2 used at a concentration of 10 microg/ml (but not of 2 microg/ml) in 8/16 diabetic patients, in 1/15 HLA-DR-matched control subjects (P<0.01 by Fisher exact test) and in 0/10 of the remaining normal individuals. A statistically significant difference (P<0.003 by Mann-Whitney U test) was also observed in S.I. values between patients (3.1+/-1.4) and HLA-DR-matched controls (1.7+/-0.54) employing IA-2 at a concentration of 10 microg/ml. However, when IA-2 was used at a concentration of 2 microg/ml, the difference in S. I. between patients (1.65+/-0.8) and controls (1.0+/-0.3) did not reach statistical significance. In conclusion, these data show the presence of a specific, dose-dependent T-lymphocyte response against the IA-2 islet tyrosine phosphatase at the onset of type 1 diabetes. Consequently, this molecule appears to be a target not only at the B-lymphocyte but also at the T-lymphocyte level, reinforcing the potential pathogenic role of this autoantigen in the islet destructive process.

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