Pancreatic NOD beta cells express MHC class II protein and the frequency of I-Ag7 mRNA-expressing beta cells strongly increases during progression to autoimmune diabetes

In the NOD mouse model, attempts to show MHC class II expression by pancreatic beta cells were unsuccessful so far. We readdressed this question by analysing I-A(g7) expression in single pancreatic beta cells. Single-cell multiplex RT PCR and single-cell immunofluorescence were used to study MHC cla...

Full description

Saved in:
Bibliographic Details
Published in:Diabetologia 2003-08, Vol.46 (8), p.1106-1114
Main Authors: WALTER, U, TOEPFER, T, VON BOEHMER, H, BUER, J, DITTMAR, K. E. J, KRETSCHMER, K, LAUBER, J, WEISS, S, SERVOS, G, LECHNER, O, SCHERBAUM, W. A, BORNSTEIN, S. R
Format: Article
Language:English
Subjects:
Antibodies
Biological and medical sciences
Biotechnology
Diabetes
Endocrinopathies
Glucose
Insulin
Laboratory animals
Lymphocytes
Medical sciences
Proteins
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:In the NOD mouse model, attempts to show MHC class II expression by pancreatic beta cells were unsuccessful so far. We readdressed this question by analysing I-A(g7) expression in single pancreatic beta cells. Single-cell multiplex RT PCR and single-cell immunofluorescence were used to study MHC class II expression in NOD and NOD/SCID beta cells. Pancreatic beta cells from NOD mice express the I-A(g7) protein as well as the corresponding mRNA. The frequency of MHC class II mRNA-expressing beta cells is drastically increased during the progression to overt diabetes. MHC class II protein is accumulated intracellularly, and invariant chain is co-expressed. Beta cells from 9- to 10-week-old NOD/SCID mice express MHC class II at the same low frequency as beta cells from 3-week-old NOD mice. NOD beta cells express I-A(g7) and could be a direct target of autoreactive CD4+ T cells. This MHC class II expression is triggered by infiltrating lymphocytes.
ISSN:0012-186X
1432-0428
DOI:10.1007/s00125-003-1164-y