Administering glutamic acid decarboxylase to NOD mice prevents diabetes.

Abstract:

:Type 1 diabetes is the result of an ongoing autoimmune response to specific proteins expressed by the insulin producing beta cells. Recently, a number of beta cell autoantigens have been identified. However, their role in mediating the diabetogenic response is not known. Here we assess the relative importance of a panel of beta cell autoantigens in the disease process. The approach was to inhibit T cell proliferation to a given autoantigen by either i.t. or i.v. injections, and then determine the effect this had on the diabetogenic response. We show that administering murine glutamic acid decarboxylase (GAD) to 3-week-old NOD females can reduce the frequency of insulitis and prevent the onset of diabetes. In contrast, carboxypeptidase H or peripherin do not induce a similar protective effect, suggesting that GAD has a critical role in the diabetogenic response. These results also suggest that GAD may provide a useful target for antigen-specific immunotherapy.

journal_name

J Autoimmun

journal_title

Journal of autoimmunity

authors

Tisch R,Yang XD,Liblau RS,McDevitt HO

doi

10.1006/jaut.1994.1067

subject

Has Abstract

pub_date

1994-12-01 00:00:00

pages

845-50

issue

6

eissn

0896-8411

issn

1095-9157

pii

S0896-8411(84)71067-5

journal_volume

7

pub_type

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