ArticleFrontiers in immunology2021
The Immunoproteasome Subunits LMP2, LMP7 and MECL-1 Are Crucial Along the Induction of Cerebral Toxoplasmosis.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- The immunoproteasome as a neuroimmune hub in the central nervous system: from proteostasis stress to inflammatory pathology.Journal of neuroinflammation · 2026Review
- Article
- Immunoproteasome Inhibition Impairs Differentiation but Not Survival of T Helper 17 Cells.Cells · 2025Article
- Immunoproteasome acted as immunotherapy 'coffee companion' in advanced carcinoma therapy.Frontiers in immunology · 2024Review
- Phytohormones regulate asexual Toxoplasma gondii replication.Parasitology research · 2023Article
- Toxoplasma gondii infection of the central nervous system and suicide: A case-control study of decedents.European journal of microbiology & immunology · 2023Article
- The neuropeptide PACAP alleviates T. gondii infection-induced neuroinflammation and neuronal impairment.Journal of neuroinflammation · 2022Article
- Airway epithelial immunoproteasome subunit LMP7 protects against rhinovirus infection.Scientific reports · 2022Article
- Immunoproteasome Inhibition Reduces the T Helper 2 Response in Mouse Models of Allergic Airway Inflammation.Frontiers in immunology · 2022Article
- Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell survival and function critically relies on the fine-tuned balance of protein synthesis and degradation. In the steady state, the standard proteasome is sufficient to maintain this proteostasis. However, upon inflammation, the sharp increase in protein production requires additional mechanisms to limit protein-associated cellular stress. Under inflammatory conditions and the release of interferons, the immunoproteasome (IP) is induced to support protein processing and recycling. In antigen-presenting cells constitutively expressing IPs, inflammation-related mechanisms contribute to the formation of MHC class I/II-peptide complexes, which are required for the induction of T cell responses. The control of
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Registered trials
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