ArticleMolecular medicine reports2018
TIPE2 governs macrophage polarization via negative regulation of mTORC1.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Review
- TIPE2 suppresses ferroptosis and pro-inflammatory polarization in macrophages triggered by SARS-CoV-2 spike protein.Scientific reports · 2025Article
- Impact of immunosuppressants on tumor pulmonary metastasis: new insight into transplantation for hepatocellular carcinoma.Cancer biology & medicine · 2024Review
- TIPE2 gene transfer ameliorates aging-associated osteoarthritis in a progeria mouse model by reducing inflammation and cellular senescence.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- TIPE2 Inhibits MGD Inflammation by Regulating Macrophage Polarization.Journal of personalized medicine · 2023Article
- TIPE2 regulates periodontal inflammation by inhibiting NF-κB p65 phosphorylation.Journal of applied oral science : revista FOB · 2023Article
- Tumor Necrosis Factor-Oxidative medicine and cellular longevity · 2022Article
- TIPE2 May Target the Nrf2/HO-1 Pathway to Inhibit M1 Macrophage-Related Neutrophilic Inflammation in Asthma.Frontiers in immunology · 2022Article
- Dendritic cells transduced with TIPE-2 recombinant adenovirus induces T cells suppression.Journal of inflammation (London, England) · 2021Article
- Transcriptomic analysis reveals that mTOR pathway can be modulated in macrophage cells by the presence of cryptococcal cells.Genetics and molecular biology · 2021Article
- Transcriptome meta-analysis reveals differences of immune profile between eutopic endometrium from stage I-II and III-IV endometriosis independently of hormonal milieu.Scientific reports · 2020Article
- Regulatory Roles of Tumor Necrosis Factor-α-Induced Protein 8 Like-Protein 2 in Inflammation, Immunity and Cancers: A Review.Cancer management and research · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages can be polarized into the inflammatory M1 lineage or the immunomodulatory M2 lineage, depending on the differential tissue microenvironment signaling, specific pathogens or cytokine stimulation. Tumor necrosis factor α‑induced protein 8‑like protein 2 (TIPE2) has been demonstrated to negatively regulate inflammation by inhibiting the Toll‑like receptor (TLR) pathway. The present study utilized murine bone marrow derived macrophages (BMDMs) as the model of undifferentiated (M0) macrophages to study the roles of TIPE2 in the differential polarization status of BMDMs. It was observed that the expression levels of TIPE2 were diminished in M1 macrophages treated with lipopolysaccharide/interferon γ, and elevated in M2 macrophages treated with interleukin (IL)‑4. BMDMs with TIPE2 overexpression exhibited defective M1 polarization and enhanced responses to IL‑4 stimulation. TIPE2 impeded M1 polarization by interfering with mitogen‑activated protein kinase kinase kinase 7‑inhibitor of nuclear factor‑κB kinase subunit β and B cell receptor‑associated protein‑serine/threonine‑protein kinase mTOR complex 1 (mTORC1) activation. TIPE2 overexpression accelerated IL‑4 induced M2 polarization by dampening mTORC1 activation via the accelerated process of arginine to urea. Overall, these results define a key role for TIPE2 in macrophage polarization by impeding mTORC1 response.
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