ArticleJournal of immunology (Baltimore, Md. : 1950)2020
4-1BBL Regulates the Polarization of Macrophages, and Inhibition of 4-1BBL Signaling Alleviates Imiquimod-Induced Psoriasis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Hyperinflammation by Human Macrophages Induced by SARS-CoV-2 Anti-Spike IgG Is Dependent on Glucose and Fatty Acid Metabolism.European journal of immunology · 2025Article
- Single-cell analysis reveals an important role of CD137L+ macrophages in the host response to uropathogenic Escherichia coli infection in the bladder.PLoS pathogens · 2025Article
- METTL3/ALKBH5-Mediated N6-Methyladenosine Modification Drives Macrophage M1 Polarization via the SLC15A3-TASL-IRF5 Signaling Axis in Psoriasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Highly differentiated T cells link systemic and vascular inflammation in a mouse model of recurrent psoriasis.Frontiers in immunology · 2025Article
- IFN-γ Induces Pleural Mesothelial Cells to Recruit Immune Cells via CXCL10-CXCR3 Axis in a Mouse Pleurisy Model.Journal of inflammation research · 2025Article
- Intratumoral delivery of lipid nanoparticle-formulated mRNA encoding IL-21, IL-7, and 4-1BBL induces systemic anti-tumor immunity.Nature communications · 2024Article
- Macrophage Functions in Psoriasis: Lessons from Mouse Models.International journal of molecular sciences · 2024Review
- Mitochondrial PGAM5-Drp1 signaling regulates the metabolic reprogramming of macrophages and regulates the induction of inflammatory responses.Frontiers in immunology · 2023Article
- Natural Plant Extract - Loganin: A Hypothesis for Psoriasis Treatment Through Inhibiting Oxidative Stress and Equilibrating Immunity via Regulation of Macrophage Polarization.Clinical, cosmetic and investigational dermatology · 2023Article
- Dynamic polarization of tumor-associated macrophages and their interaction with intratumoral T cells in an inflamed tumor microenvironment: from mechanistic insights to therapeutic opportunities.Frontiers in immunology · 2023Review
- MicroRNA-22 Regulates the Pro-inflammatory Responses and M1 Polarization of Macrophages by Targeting GLUT1 and 4-1BBL.Journal of immunology research · 2023Article
- Calcium/calmodulin-dependent protein kinase IV promotes imiquimod-induced psoriatic inflammation via macrophages and keratinocytes in mice.Nature communications · 2022Article
- Shikonin combined with methotrexate regulate macrophage polarization to treat psoriasis.Bioengineered · 2022Article
- Dendritic Cells and Macrophages in the Pathogenesis of Psoriasis.Frontiers in immunology · 2022Review
- Fa(c)t checking: How fatty acids shape metabolism and function of macrophages and dendritic cells.European journal of immunology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
4-1BBL, a member of the TNF superfamily, regulates the sustained production of inflammatory cytokines in macrophages triggered by TLR signaling. In this study, we have investigated the role of 4-1BBL in macrophage metabolism and polarization and in skin inflammation using a model of imiquimod-induced psoriasis in mice. Genetic ablation or blocking of 4-1BBL signaling by Ab or 4-1BB-Fc alleviated the pathology of psoriasis by regulating the expression of inflammatory cytokines associated with macrophage activation and regulated the polarization of macrophages in vitro. We further linked this result with macrophage by finding that 4-1BBL expression during the immediate TLR response was dependent on glycolysis, mitochondrial oxidative phosphorylation, and fatty acid metabolism, whereas the late-phase 4-1BBL-mediated sustained inflammatory response was dependent on glycolysis and fatty acid synthesis. Correlating with this, administration of a fatty acid synthase inhibitor, cerulenin, also alleviated the pathology of psoriasis. We further found that 4-1BBL-mediated psoriasis development is independent of its receptor 4-1BB, as a deficiency of 4-1BB augmented the severity of psoriasis linked to a reduced regulatory T cell population and increased IL-17A expression in γδ T cells. Additionally, coblocking of 4-1BBL signaling and IL-17A activity additively ameliorated psoriasis. Taken together, 4-1BBL signaling regulates macrophage polarization and contributes to imiquimod-induced psoriasis by sustaining inflammation, providing a possible avenue for psoriasis treatment in patients.
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Registered trials
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