ArticleProceedings of the National Academy of Sciences of the United States of America2008
PD-1 deficiency reveals various tissue-specific autoimmunity by H-2b and dose-dependent requirement of H-2g7 for diabetes in NOD mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 46 citations in OpenAlex.
- Spontaneous organ-specific eye autoimmune disease resulting from two engineered gene mutations compromising immune tolerance.Frontiers in immunology · 2026Review
- Immune checkpoint imbalance in ANCA-associated vasculitis: insights into disease activity and precision immunotherapy.Frontiers in medicine · 2026Review
- Animal models of immune-mediated demyelinating polyneuropathies.Autoimmunity · 2024Review
- Murine MHC-Deficient Nonobese Diabetic Mice Carrying Human HLA-DQ8 Develop Severe Myocarditis and Myositis in Response to Anti-PD-1 Immune Checkpoint Inhibitor Cancer Therapy.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- PD-1 expression in tumor infiltrating lymphocytes as a prognostic marker in early-stage non-small cell lung cancer.Frontiers in oncology · 2024Article
- Review
- Spatial transcriptomics of the lacrimal gland features macrophage activity and epithelium metabolism as key alterations during chronic inflammation.Frontiers in immunology · 2022Article
- The NOD Mouse Beyond Autoimmune Diabetes.Frontiers in immunology · 2022Review
- Review
- Not-so-opposite ends of the spectrum: CD8Nature immunology · 2021Review
- A snapshot of the PD-1/PD-L1 pathway.Journal of Cancer · 2021Review
- Programmed cell death-1Journal of translational autoimmunity · 2021Article
- T Cells from NOD-Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Deciphering immune mechanisms in chronic inflammatory demyelinating polyneuropathies.JCI insight · 2020Review
- Novel pathomechanisms in inflammatory neuropathies.Journal of neuroinflammation · 2017Review
- Molecular and Biochemical Aspects of the PD-1 Checkpoint Pathway.The New England journal of medicine · 2016Review
- Immune checkpoint therapy and type 1 diabetes.Diabetology international · 2016Article
- PD-1 expression on dendritic cells suppresses CD8Oncoimmunology · 2016Article
- T-bet regulates differentiation of forkhead box protein 3+ regulatory T cells in programmed cell death-1-deficient mice.Clinical and experimental immunology · 2015Article
- CD19 as a therapeutic target in a spontaneous autoimmune polyneuropathy.Clinical and experimental immunology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although many autoimmune diseases are associated with particular HLA/H-2 haplotypes, the mechanisms through which specific HLA/H-2 haplotypes afford autoimmune susceptibility remain enigmatic. Here, we analyzed the effects of the diabetes-associated (H-2(g7)) and an antidiabetogenic (H-2(b)) H-2 haplotypes in NOD mice deficient for programmed cell death-1 (PD-1, Pdcd1), a unique model of type 1 diabetes that confers complete penetrance and rapid onset of the disease. NOD-H2(b/b)Pdcd1(-/-) mice were completely protected from diabetes, confirming that H-2(g7) is indispensable for diabetes even in the absence of PD-1. However, NOD-H2(b/b)Pdcd1(-/-) mice developed autoimmune inflammation in multiple tissues including peripheral nerves, stomachs, and exocrine tissues, demonstrating that autoreactive T cells are generated in the context of H-2(b). These autoreactive T cells damaged target tissues only in the absence of PD-1, confirming that PD-1 deficiency unravels the hidden autoimmune susceptibility of the strain by reducing the threshold of T cell activation. Transfer experiments revealed that CD4 T cells are the effector cells of neuritis, and nerve-infiltrating CD4 T cells are strongly deviated toward Th1. Interestingly, neuritogenic T cells were also generated in the context of H-2(g7), in sharp contrast to the strict requirement of H-2(g7) for diabetes. In addition, 60% of the NOD-H2(b/g7)Pdcd1(-/-) mice developed diabetes, suggesting that H-2(b) does not dominantly suppress diabetes and that H-2(g7) induces diabetes in a dose-dependent fashion.
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