ArticleFrontiers in immunology2017
Cathepsin E Deficiency Ameliorates Graft-versus-Host Disease and Modifies Dendritic Cell Motility.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Cathepsin Family Proteases in Prodrug Design: Recent Advances.ChemMedChem · 2026Review
- Review
- A novel efferocytosis-related gene signature for predicting prognosis and therapeutic response in bladder cancer.Scientific reports · 2025Article
- Bioinformatics-based screening of key genes associated with gemcitabine resistance in advanced pancreatic ductal adenocarcinoma.Translational cancer research · 2024Article
- MERTK inhibition selectively activates a DC - T-cell axis to provide anti-leukemia immunity.Leukemia · 2024Article
- Article
- Spatio-Temporal Bone Remodeling after Hematopoietic Stem Cell Transplantation.International journal of molecular sciences · 2020Article
- Reduced Calcium Signaling Is Associated With Severe Graft-Versus-Host Disease: Results From Preclinical Models and From a Prospective EBMT Study.Frontiers in immunology · 2020Article
- Innate Immune Determinants of Graft-Versus-Host Disease and Bidirectional Immune Tolerance in Allogeneic Transplantation.OBM transplantation · 2019Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microbial products influence immunity after allogeneic hematopoietic stem cell transplantation (allo-SCT). In this context, the role of cathepsin E (Ctse), an aspartate protease known to cleave bacterial peptides for antigen presentation in dendritic cells (DCs), has not been studied. During experimental acute graft-versus-host disease (GVHD), we found infiltration by Ctse-positive immune cells leading to higher Ctse RNA- and protein levels in target organs. In Ctse-deficient allo-SCT recipients, we found ameliorated GVHD, improved survival, and lower numbers of tissue-infiltrating DCs. Donor T cell proliferation was not different in Ctse-deficient vs. wild-type allo-SCT recipients in MHC-matched and MHC-mismatched models. Furthermore, Ctse-deficient DCs had an intact ability to induce allogeneic T cell proliferation, suggesting that its role in antigen presentation may not be the main mechanism how Ctse impacts GVHD. We found that Ctse deficiency significantly decreases DC motility
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