ArticleNature communications2018
Peli1 negatively regulates noncanonical NF-κB signaling to restrain systemic lupus erythematosus.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 70 citations in OpenAlex.
- Expanded but dysfunctional regulatory T cells in treatment-naïve autoimmune hepatitis.Hepatology international · 2026Article
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Peli1, regulated by mCommunications biology · 2025Article
- A novel missense variant in TNFAIP3 associated with autoimmunity reveals the contribution of STAT1/mTOR pathways.Clinical and experimental immunology · 2025Article
- Ubiquitin-proteasome system: a potential participant and therapeutic target in antiphospholipid syndrome.Frontiers in immunology · 2025Review
- [Immunological status in patients with amenorrhea (literature review)].Problemy endokrinologii · 2024Review
- Gasdermin D deficiency aborts myeloid calcium influx to drive granulopoiesis in lupus nephritis.Cell communication and signaling : CCS · 2024Article
- The role of mesenchymal stem cells in attenuating inflammatory bowel disease through ubiquitination.Frontiers in immunology · 2024Review
- The Immune Modulatory Role of TIF1 Proteins.Advances in experimental medicine and biology · 2024Review
- Enrichment of a neutrophil-like monocyte transcriptional state in glioblastoma myeloid suppressor cells.Research square · 2023Article
- The Role of Ubiquitin-Proteasome System and Mitophagy in the Pathogenesis of Parkinson's Disease.Neuromolecular medicine · 2023Review
- Cytoplasmic DNA sensing boosts CD4Life medicine · 2023Article
- Goliath induces inflammation in obese mice by linking fatty acid β-oxidation to glycolysis.EMBO reports · 2023Article
- Deciphering the role of cDC2s in Sjögren's syndrome: transcriptomic profile links altered antigen processes with IFN signature and autoimmunity.Annals of the rheumatic diseases · 2023Article
- Review
- Decreased Peli1 expression attenuates osteoarthritis by protecting chondrocytes and inhibiting M1-polarization of macrophages.Bone & joint research · 2023Article
- A quinazoline derivative suppresses B cell hyper-activation and ameliorates the severity of systemic lupus erythematosus in mice.Frontiers in pharmacology · 2023Article
- Biology of Pellino1: a potential therapeutic target for inflammation in diseases and cancers.Frontiers in immunology · 2023Review
- Article
- A ceRNA regulatory network in systemic lupus erythematosus and its molecular interplay with cancer.Annals of translational medicine · 2022Article
Corrections and comments
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Authors and funding
22 authors at 6 institutions in 2 countries.
Funding
Abstract
Systemic lupus erythematosus (SLE) is characterized by uncontrolled secretion of autoantibodies by plasma cells. Although the functional importance of plasma cells and autoantibodies in SLE has been well established, the underlying molecular mechanisms of controlling autoantibody production remain poorly understood. Here we show that Peli1 has a B cell-intrinsic function to protect against lupus-like autoimmunity in mice. Peli1 deficiency in B cells induces autoantibody production via noncanonical NF-κB signaling. Mechanically, Peli1 functions as an E3 ligase to associate with NF-κB inducing kinase (NIK) and mediates NIK Lys48 ubiquitination and degradation. Overexpression of Peli1 inhibits noncanonical NF-κB activation and alleviates lupus-like disease. In humans, PELI1 levels negatively correlate with disease severity in SLE patients. Our findings establish Peli1 as a negative regulator of the noncanonical NF-κB pathway in the context of restraining the pathogenesis of lupus-like disease.
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Registered trials
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