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Article

Peripheral T cell clones from NOD mice specific for GAD65 peptides: lack of islet responsiveness or diabetogenicity.

Journal of autoimmunity - 1 Jun 1996

Schloot N C, Daniel D, Norbury-Glaser M, Wegmann D R

Abstract excerpt

The non-obese diabetic (NOD) mouse develops diabetes as a result of spontaneous T cell mediated destruction of the insulin-producing beta-cells. Tolerization to glutamic acid decarboxylase (GAD65) has been reported to inhibit spontaneous T cell proliferative responses to GAD65 and GAD65 peptides and prevent insulitis and diabetes in NOD mice. To evaluate the role of T cells responsive to GAD65 in induction of...

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Identifiers

PMID: 8816971
DOI: 10.1006/jaut.1996.0048

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Peripheral T cell clones from NOD mice specific for GAD65 peptides: lack of islet responsiveness or diabetogenicity.PMID 8816971Read ↗

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