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Article

Defects in the differentiation and function of antigen presenting cells in NOD/Lt mice.

Journal of immunology (Baltimore, Md. : 1950) - 15 Mar 1993

Serreze D V, Gaskins H R, Leiter E H

Abstract excerpt

Although T lymphocytes are the ultimate effectors of pancreatic beta cell destruction in autoimmune insulin-dependent diabetes, previous work has established that beta cell autoreactive T cells are generated in nonobese diabetic (NOD) mice as a result of APC dysfunctions. To determine if APC dysfunctions could result from developmental defects, we analyzed if macrophages (M phi) develop normally from NOD bone...

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Source

Identifiers

PMID: 8450229

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APC

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Defects in the differentiation and function of antigen presenting cells in NOD/Lt mice.PMID 8450229Read ↗

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Idd9/11 genetic locus regulates diabetogenic activity of CD4 T-cells in nonobese diabetic (NOD) mice.Semantic proximity Read ↗

Dysregulated B7-1 and B7-2 expression on nonobese diabetic mouse B cells is associated with increased T cell costimulation and the development of insulitis.Semantic proximity Read ↗

NOD mice and autoimmunity.Semantic proximity Read ↗

Interferon-gamma receptor signaling is dispensable in the development of autoimmune type 1 diabetes in NOD mice.Semantic proximity Read ↗

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Islet-infiltrating T cell clones from non-obese diabetic mice that promote or prevent accelerated onset diabetes.Semantic proximity Read ↗

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