ArticleLife science alliance2019
Distinct signals and immune cells drive liver pathology and glomerulonephritis in ABIN1[D485N] mice.
Article in Life science alliance, 2019. 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, 21 citations in OpenAlex.
- A TNIP1-driven systemic autoimmune disorder with elevated IgG4.Nature immunology · 2024Article
- ABIN1 is a negative regulator of effector functions in cytotoxic T cells.EMBO reports · 2024Article
- Attenuation of HOIL-1L ligase activity promotes systemic autoimmune disorders by augmenting linear ubiquitin signaling.JCI insight · 2024Article
- Germinal center versus extrafollicular responses in systemic autoimmunity: Who turns the blade on self?Advances in immunology · 2024Review
- Pacritinib abrogates the lupus phenotype in ABIN1[D485N] mice.Lupus science & medicine · 2023Article
- Identification of ester-linked ubiquitylation sites during TLR7 signalling increases the number of inter-ubiquitin linkages from 8 to 12.The Biochemical journal · 2022Article
- Ubiquitin-binding domain in ABIN1 is critical for regulating cell death and inflammation during development.Cell death and differentiation · 2022Article
- TAK1 protein kinase activity is required for TLR signalling and cytokine production in myeloid cells.The Biochemical journal · 2022Article
- Analysis of the Expression of Neurotrophins and Their Receptors in Adult Zebrafish Kidney.Veterinary sciences · 2022Article
- Article
- Prevention and partial reversion of the lupus phenotype in ABIN1[D485N] mice by an IRAK4 inhibitor.Lupus science & medicine · 2021Article
- LUBAC-mediated linear ubiquitination: a crucial regulator of immune signaling.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2021Review
- Review
- Precision Targeting of NF-κB Signaling in Lupus Nephritis.Lupus (Los Angeles) · 2020Article
- Functional Metabolomics Analysis Elucidating the Metabolic Biomarker and Key Pathway Change Associated With the Chronic Glomerulonephritis and Revealing Action Mechanism of Rhein.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
We report that TLR7, IL-6, and the adaptive immune system are essential for autoimmunity and glomerulonephritis but not for liver pathology in mice expressing the ubiquitin-binding-defective ABIN1[D485N] mutant. The blood and organs of ABIN1[D485N] mice have exceptionally high numbers of patrolling monocytes (pMo), which develop independently of IL-6 and the adaptive immune system. They are detectable in the blood months before autoimmunity and organ pathology are seen and may have diagnostic potential. The splenic pMo, inflammatory monocytes (iMo), and neutrophils of ABIN1[D485N] mice expressed high levels of mRNAs encoding proteins released during NETosis, which together with the high numbers of monocyte-derived dendritic cells (MoDCs) may drive the liver pathology in ABIN1[D485N] mice, and contribute to the pathology of other organs. The splenic iMo of ABIN1[D485N] mice displayed high expression of mRNAs encoding proteins controlling cell division and were actively dividing; this may underlie the increased pMo and MoDC numbers, which are derived from iMo. An orally active IRAK4 inhibitor suppressed all facets of the disease phenotype and prevented the increase in pMo numbers.
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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.