ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Cathepsin B controls the persistence of memory CD8+ T lymphocytes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Cytosolic serpins act in a cytoprotective feedback loop that limits ESX-1-dependent death ofmBio · 2024Article
- Combined PD-L1/TGFβ blockade allows expansion and differentiation of stem cell-like CD8 T cells in immune excluded tumors.Nature communications · 2023Article
- NNature communications · 2023Article
- Cysteine Cathepsins as Therapeutic Targets in Immune Regulation and Immune Disorders.Biomedicines · 2023Review
- The Role of Cathepsin B in Pathophysiologies of Non-tumor and Tumor tissues: A Systematic Review.Journal of Cancer · 2023Review
- Duodenal CD8+ T resident memory cell apoptosis contributes to gut barrier dysfunction and microbial translocation in early alcohol-associated liver disease in humans.Alimentary pharmacology & therapeutics · 2022Article
- Spatial localization of cathepsins: Implications in immune activation and resolution during infections.Frontiers in immunology · 2022Review
- The Serpin Superfamily and Their Role in the Regulation and Dysfunction of Serine Protease Activity in COPD and Other Chronic Lung Diseases.International journal of molecular sciences · 2021Review
- The Role of Cysteine Peptidases in Hematopoietic Stem Cell Differentiation and Modulation of Immune System Function.Frontiers in immunology · 2021Review
- Early emergence of T central memory precursors programs clonal dominance during chronic viral infection.Nature immunology · 2020Article
- Novel Opportunities for Cathepsin S Inhibitors in Cancer Immunotherapy by Nanocarrier-Mediated Delivery.Cells · 2020Review
- Cysteinyl cathepsins in cardiovascular diseases.Biochimica et biophysica acta. Proteins and proteomics · 2020Review
- IL-27 promotes the expansion of self-renewing CD8The Journal of experimental medicine · 2019Article
- Cysteine Cathepsins in Tumor-Associated Immune Cells.Frontiers in immunology · 2019Review
- Cysteine-type cathepsins promote the effector phase of acute cutaneous delayed-type hypersensitivity reactions.Theranostics · 2019Article
- Antiapoptotic serine protease inhibitors contribute to survival of allergenic TThe Journal of allergy and clinical immunology · 2018Article
- Cysteine protease cathepsins in cardiovascular disease: from basic research to clinical trials.Nature reviews. Cardiology · 2018Review
- Multiple signals at the extended 8p23 locus are associated with susceptibility to systemic lupus erythematosus.Journal of medical genetics · 2017Article
- Cathepsin B-Deficient Mice Resolve Leishmania major Inflammation Faster in a T Cell-Dependent Manner.PLoS neglected tropical diseases · 2016Article
- Stemness of T cells and the hematopoietic stem cells: fate, memory, niche, cytokines.Cytokine & growth factor reviews · 2013Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The persistence of memory T lymphocytes confers lifelong protection from pathogens. Memory T cells survive and undergo homeostatic proliferation (HSP) in the absence of Ag, although the cell-intrinsic mechanisms by which cytokines drive the HSP of memory T cells are not well understood. In this study we report that lysosome stability limits the long-term maintenance of memory CD8(+) T cell populations. Serine protease inhibitor (Spi) 2A, an anti-apoptotic cytosolic cathepsin inhibitor, is induced by both IL-15 and IL-7. Mice deficient in Spi2A developed fewer memory phenotype CD44(hi)CD8(+) T cells with age, which underwent reduced HSP in the bone marrow. Spi2A was also required for the maintenance of central memory CD8(+) T cell populations after acute infection with lymphocytic choriomeningitis virus. Spi2A-deficient Ag-specific CD8(+) T cell populations declined more than wild-type competitors after viral infection, and they were eroded further after successive infections. Spi2A protected memory cells from lysosomal breakdown by inhibiting cathepsin B. The impaired maintenance of Spi2A-deficient memory CD8(+) T cells was rescued by concomitant cathepsin B deficiency, demonstrating that cathepsin B was a physiological target of Spi2A in memory CD8(+) T cell survival. Our findings support a model in which protection from lysosomal rupture through cytokine-induced expression of Spi2A determines the long-term persistence of memory CD8(+) T cells.
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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.