ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Cutting Edge: defective follicular exclusion of apoptotic antigens due to marginal zone macrophage defects in autoimmune BXD2 mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
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- Macrophages Unmasked: Their Pivotal Role in Driving Atherosclerosis in Systemic Lupus Erythematosus.Clinical reviews in allergy & immunology · 2025Review
- Immunological control of skin development: from homeostasis to developmental pathologies.Frontiers in immunology · 2025Review
- The role of autoantibodies in bridging obesity, aging, and immunosenescence.Immunity & ageing : I & A · 2024Review
- Roles of macrophages in lupus nephritis.Frontiers in pharmacology · 2024Review
- Increased development of T-betClinical immunology (Orlando, Fla.) · 2023Article
- Macrophage: Key player in the pathogenesis of autoimmune diseases.Frontiers in immunology · 2023Review
- Coordination between innate immune cells, type I IFNs and IRF5 drives SLE pathogenesis.Cytokine · 2020Review
- Systemic lupus erythematosus favors the generation of IL-17 producing double negative T cells.Nature communications · 2020Article
- Autoreactive B cells in SLE, villains or innocent bystanders?Immunological reviews · 2019Review
- Predominant Role of Immunoglobulin G in the Pathogenesis of Splenomegaly in Murine Lupus.Frontiers in immunology · 2019Article
- Marginal Zone B Cells Induce Alloantibody Formation Following RBC Transfusion.Frontiers in immunology · 2018Article
- The contribution of the programmed cell death machinery in innate immune cells to lupus nephritis.Clinical immunology (Orlando, Fla.) · 2017Review
- Pathogenesis of Human Systemic Lupus Erythematosus: A Cellular Perspective.Trends in molecular medicine · 2017Review
- B cell contribution of the CD4Autoimmunity · 2017Review
- The CD169 sialoadhesin molecule mediates cytotoxic T-cell responses to tumour apoptotic vesicles.Immunology and cell biology · 2016Article
- Apoptotic cell responses in the splenic marginal zone: a paradigm for immunologic reactions to apoptotic antigens with implications for autoimmunity.Immunological reviews · 2016Review
- The many faces of type I interferon in systemic lupus erythematosus.The Journal of clinical investigation · 2015Article
- Interferon-induced mechanosensing defects impede apoptotic cell clearance in lupus.The Journal of clinical investigation · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Marginal zone macrophages (MZMs) act as a barrier to entry of circulating apoptotic debris into the follicles of secondary lymphoid organs. In autoimmune BXD2 mice, there is a progressive reduction in the function and numbers of MZMs. Absence of MZMs results in retention of apoptotic cell (AC) debris within the marginal zone (MZ) and increased loading of AC Ags on MZ B cells and MZ-precursor (MZ-P) B cells. The MZ-P B cells are capable of translocating the AC Ags to the follicular zone and stimulating T cells. Both MZMs and MZ-P B cells from BXD2 mice express low levels of tolerogenic signals and high levels of inflammatory signals. Thus, the current study suggests a multifaceted mechanism in which MZMs maintain tolerance to apoptotic autoantigens and suppress their translocation to follicles. Lack of clearance of apoptotic debris by MZMs drives follicular Ag-transportation by MZ-P B cells to stimulate an autoimmune response.
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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.