ArticleThe Journal of clinical investigation2015
Interferon-induced mechanosensing defects impede apoptotic cell clearance in lupus.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
- Autoimmunity and peginterferon therapy for polycythemia vera.HemaSphere · 2026Review
- Targeting TKT-associated immunometabolic remodeling attenuates experimental lupus nephritis and NET-related inflammation.Frontiers in cell and developmental biology · 2026Article
- Defining the Role of Marginal Zone B Cells in FVIII Inhibitor Development.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Efferocytosis in Health and Disease.MedComm · 2025Review
- IL-4 alters TLR7-induced B cell developmental program in lupus.Clinical immunology (Orlando, Fla.) · 2025Article
- Efferocytosis in Homeostasis.Advances in experimental medicine and biology · 2025Review
- The Aconitate Decarboxylase 1/Itaconate Pathway Modulates Immune Dysregulation and Associates with Cardiovascular Disease Markers and Disease Activity in Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Integrin αvβ3 Limits Cytokine Production by Plasmacytoid Dendritic Cells and Restricts TLR-Driven Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- The aconitate decarboxylase 1/itaconate pathway modulates immune dysregulation and associates with cardiovascular disease markers in SLE.medRxiv : the preprint server for health sciences · 2024Article
- How underappreciated autoinflammatory (innate immunity) mechanisms dominate disparate autoimmune disorders.Frontiers in immunology · 2024Review
- Increased development of T-betClinical immunology (Orlando, Fla.) · 2023Article
- Macrophage: Key player in the pathogenesis of autoimmune diseases.Frontiers in immunology · 2023Review
- IL-4 receptor blockade is a global repressor of naïve B cell development and responses in a dupilumab-treated patient.Clinical immunology (Orlando, Fla.) · 2022Article
- Lupus nephritis correlates with B cell interferon-β, anti-Smith, and anti-DNA: a retrospective study.Arthritis research & therapy · 2022Article
- Host Genetics But Not Commensal Microbiota Determines the Initial Development of Systemic Autoimmune Disease in BXD2 Mice.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
- Regulation of B Cell Responses in SLE by Three Classes of Interferons.International journal of molecular sciences · 2021Review
- B cell subset composition segments clinically and serologically distinct groups in chronic cutaneous lupus erythematosus.Annals of the rheumatic diseases · 2021Article
- IL-23 reshapes kidney resident cell metabolism and promotes local kidney inflammation.The Journal of clinical investigation · 2021Article
- Association Between a History of NontyphoidalFrontiers in immunology · 2021Article
- Systemic lupus erythematosus favors the generation of IL-17 producing double negative T cells.Nature communications · 2020Article
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14 authors at 7 institutions in 3 countries.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a severe autoimmune disease that is associated with increased circulating apoptotic cell autoantigens (AC-Ags) as well as increased type I IFN signaling. Here, we describe a pathogenic mechanism in which follicular translocation of marginal zone (MZ) B cells in the spleens of BXD2 lupus mice disrupts marginal zone macrophages (MZMs), which normally clear AC debris and prevent follicular entry of AC-Ags. Phagocytosis of ACs by splenic MZMs required the megakaryoblastic leukemia 1 (MKL1) transcriptional coactivator-mediated mechanosensing pathway, which was maintained by MZ B cells through expression of membrane lymphotoxin-α1β2 (mLT). Specifically, type I IFN-induced follicular shuttling of mLT-expressing MZ B cells disengaged interactions between these MZ B cells and LTβ receptor-expressing MZMs, thereby downregulating MKL1 in MZMs. Loss of MKL1 expression in MZMs led to defective F-actin polymerization, inability to clear ACs, and, eventually, MZM dissipation. Aggregation of plasmacytoid DCs in the splenic perifollicular region, follicular translocation of MZ B cells, and loss of MKL1 and MZMs were also observed in an additional murine lupus model and in the spleens of patients with SLE. Collectively, the results suggest that lupus might be interrupted by strategies that maintain or enhance mechanosensing signaling in the MZM barrier to prevent follicular entry of AC-Ags.
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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.