ArticleThe Journal of clinical investigation2005
Cathepsin L is essential for onset of autoimmune diabetes in NOD mice.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 88 citations in OpenAlex.
- CTSH regulates β-cell function and disease progression in newly diagnosed type 1 diabetes patients.Proceedings of the National Academy of Sciences of the United States of America · 2014Trial
- Effect of the S2' site cleavage on SARS-CoV-2 spike.Nature communications · 2025Article
- Let the CAThepsin L out of the thymus.Nature immunology · 2025Article
- SARS-CoV-2 spike protein: structure, viral entry and variants.Nature reviews. Microbiology · 2025Review
- Potential Effects of Hyperglycemia on SARS-CoV-2 Entry Mechanisms in Pancreatic Beta Cells.Viruses · 2024Review
- Impact of the Warhead of Dipeptidyl Keto Michael Acceptors on the Inhibition Mechanism of Cysteine Protease Cathepsin L.ACS catalysis · 2023Article
- System analysis based on the lysosome-related genes identifies HPS4 as a novel therapy target for liver hepatocellular carcinoma.Frontiers in oncology · 2023Article
- Challenges and opportunities in analyzing and modeling peptide presentation by HLA-II proteins.Frontiers in immunology · 2023Article
- Cathepsin D Drives the Formation of Hybrid Insulin Peptides Relevant to the Pathogenesis of Type 1 Diabetes.Diabetes · 2022Article
- Going viral in the islet: mediators of SARS-CoV-2 entry beyond ACE2.Journal of molecular endocrinology · 2022Review
- Transcriptomic and metabolomic associations with exposures to air pollutants among young adults with childhood asthma history.Environmental pollution (Barking, Essex : 1987) · 2022Article
- The Role of Proteases and Serpin Protease Inhibitors in β-Cell Biology and Diabetes.Biomolecules · 2022Review
- Article
- Lysosomal cathepsin creates chimeric epitopes for diabetogenic CD4 T cells via transpeptidation.The Journal of experimental medicine · 2021Article
- Hidden in Plain View: Discovery of Chimeric Diabetogenic CD4 T Cell Neo-Epitopes.Frontiers in immunology · 2021Review
- A Review of Small Molecule Inhibitors and Functional Probes of Human Cathepsin L.Molecules (Basel, Switzerland) · 2020Review
- Cathepsin L in COVID-19: From Pharmacological Evidences to Genetics.Frontiers in cellular and infection microbiology · 2020Review
- The Role of T Cell Receptor Signaling in the Development of Type 1 Diabetes.Frontiers in immunology · 2020Review
- Cellular proliferation in mouse and human pancreatic islets is regulated by serpin B13 inhibition and downstream targeting of E-cadherin by cathepsin L.Diabetologia · 2019Article
- Engineered nanomaterial-induced lysosomal membrane permeabilization and anti-cathepsin agents.Journal of toxicology and environmental health. Part B, Critical reviews · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Lysosomal proteases generate peptides presented by class II MHC molecules to CD4+ T cells. To determine whether specific lysosomal proteases might influence the outcome of a CD4+ T cell-dependent autoimmune response, we generated mice that lack cathepsin L (Cat L) on the autoimmune diabetes-prone NOD inbred background. The absence of Cat L affords strong protection from disease at the stage of pancreatic infiltration. The numbers of I-A(g7)-restricted CD4+ T cells are diminished in Cat L-deficient mice, although a potentially diabetogenic T cell repertoire persists. Within the CD4+ T cell compartments of Cat L-deficient mice, there is an increased proportion of regulatory T cells compared with that in Cat L-sufficient littermates. We suggest that it is this displaced balance of regulatory versus aggressive CD4+ T cells that protects Cat L-deficient mice from autoimmune disease. Our results identify Cat L as an enzyme whose activity is essential for the development of type I diabetes in the NOD mouse.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.