ArticleMediators of inflammation2013
Blockade of 4-1BB and 4-1BBL interaction reduces obesity-induced skeletal muscle inflammation.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- 4-1BB: A promising target for cancer immunotherapy.Frontiers in oncology · 2022Review
- Ectopic CD137 expression by rhabdomyosarcoma provides selection advantages but allows immunotherapeutic targeting.Oncoimmunology · 2021Article
- 4-1BBL Regulates the Polarization of Macrophages, and Inhibition of 4-1BBL Signaling Alleviates Imiquimod-Induced Psoriasis.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- The involvement of 4-1BB/4-1BBL signaling in glial cell-mediated hypothalamic inflammation in obesity.FEBS open bio · 2018Article
- Interglial Crosstalk in Obesity-Induced Hypothalamic Inflammation.Frontiers in neuroscience · 2018Review
- Absence of 4-1BB reduces obesity-induced atrophic response in skeletal muscle.Journal of inflammation (London, England) · 2017Article
- Inhibition of 4-1BBL-regulated TLR response in macrophages ameliorates endotoxin-induced sepsis in mice.European journal of immunology · 2015Article
- 4-1BB Agonists: Multi-Potent Potentiators of Tumor Immunity.Frontiers in oncology · 2015Review
- Quercetin protects against obesity-induced skeletal muscle inflammation and atrophy.Mediators of inflammation · 2014Article
- Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity-induced skeletal muscle inflammation is characterized by increased macrophage infiltration and inflammatory cytokine production. In this study, we investigated whether 4-1BB, a member of the TNF receptor superfamily (TNFRSF9) that provides inflammatory signals, participates in obesity-induced skeletal muscle inflammation. Expression of the 4-1BB gene, accompanied by increased levels of inflammatory cytokines, was markedly upregulated in the skeletal muscle of obese mice fed a high-fat diet, in muscle cells treated with obesity factors, and in cocultured muscle cells/macrophages. In vitro stimulation of 4-1BB with agonistic antibody increased inflammatory cytokine levels in TNFα-pretreated muscle cells, and this effect was absent in cells derived from 4-1BB-deficient mice. Conversely, disruption of the interaction between 4-1BB and its ligand (4-1BBL) with blocking antibody decreased the release of inflammatory cytokines from cocultured muscle cells/macrophages. Moreover, deficiency of 4-1BB markedly reduced macrophage infiltration and inflammatory cytokine production in the skeletal muscle of mice fed a high-fat diet. These findings indicate that 4-1BB mediates the inflammatory responses in obese skeletal muscle by interacting with its ligand 4-1BBL on macrophages. Therefore, 4-1BB and 4-1BBL may be useful targets for prevention of obesity-induced inflammation in skeletal muscle.
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