ReviewFrontiers in immunology2025
Elucidating the immunomodulatory roles and mechanisms of CUL4B in the immune system: a comprehensive review.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Damage-Associated Molecular Patterns in Mesothelioma: Drivers of Inflammation and Therapeutic Targets.International journal of molecular sciences · 2026Review
- The Roles of E3 Ubiquitin Ligases in Cerebral Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cullin 4B (CUL4B), a pivotal member of the Cullins protein family, plays a crucial role in immune regulation and has garnered significant research attention. CUL4B, through the Cullin 4B-RING E3 ubiquitin ligase (CRL4B) complex, regulates CD4+ T cell differentiation, fostering a balance between TH1 and TH2 subsets, and expedites DNA damage repair to bolster T cell persistence. In B cells, CUL4B upregulation stimulates immune responses but is linked to an unfavorable prognosis in lymphoma. In innate immunity, CUL4B modulates Toll-like receptor (TLR)-mediated anti-inflammatory responses, enhancing macrophage migration and adhesion. CUL4B also plays a role in potentiating anti-tumor immunity by restricting the activity of myeloid-derived suppressor cells (MDSCs). In disease pathogenesis, CUL4B limits MDSCs to enhance anti-tumor effects, and its inhibition in experimental autoimmune encephalomyelitis (EAE) models have demonstrated beneficial effects, underscoring its potential therapeutic significance in autoimmune diseases. Furthermore, CUL4B is involved in various immune-related cancers and inflammation, including pleural mesothelioma, human osteosarcoma, and colitis-associated cancer. In metabolic diseases, CUL4B regulates adipose tissue and insulin sensitivity, with its depletion improving metabolic phenotypes. This review highlights the pivotal role of CUL4B in maintaining immune homeostasis and provides novel perspectives and insights into the understanding and development of treatments for immune-related disorders.
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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.