The NOD mouse: a model of immune dysregulation.

By Mark S. Anderson, J. Bluestone. Annual Review of Immunology, 2005

1,199 citations recorded by the source corpus.

Subfields: Genetics, Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/4657fa94a5dee3bdc5bfa7e26224d5819b7c05dd

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In Genetics

1. B. Fife
2. J. Bluestone

In Immunology

1. J. Bluestone
2. B. Fife
3. Q. Tang
4. C. Piccirillo
5. J. Buckner
6. Shimon Sakaguchi
7. E. Shevach

In Surgery

1. J. Bluestone

Citations in the corpus

• Control of peripheral T‐cell tolerance and autoimmunity via the CTLA‐4 and PD‐1 pathways (2008, background): “In PD-1-sufficient NOD mice, infiltrating T cells form a cluster surrounding the pancreatic islets (peri-insulitis) and rarely invade the islets, forming a ring as if there were a protective barrier (93).”
• The Role of Inflammation in Diabetes: Current Concepts and Future Perspectives (2018, positive): “, demonstrated that failure in both central and peripheral immune tolerance mechanisms contribute to the emergence of autoreactive T cells in the periphery of non-obese mice with diabetes.(31) Regulatory T cells (Tregs) have been shown to also be defective in this autoimmune disease setting, along w”
• Central role of defective interleukin-2 production in the triggering of islet autoimmune destruction. (2008, background): “and tissue destruction progress asynchronously in different islets ( Anderson and Bluestone, 2005 ), confocal microscopic analyses of immunofluorescent antibody-stained pancreatic sections were performed to characterize the Foxp3+CD4+ Treg”