ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Selective Memory to Apoptotic Cell-Derived Self-Antigens with Implications for Systemic Lupus Erythematosus Development.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 22 citations in OpenAlex.
- Unveiling the hidden role of the interaction between CD36 and FcγRIIb: implications for autoimmune disorders.Cellular & molecular biology letters · 2024Article
- LAMP3 induces apoptosis and autoantigen release in Sjögren's syndrome patients.Scientific reports · 2020Article
- Precocious expression of Blimp1 in B cells causes autoimmune disease with increased self-reactive plasma cells.The EMBO journal · 2019Article
- Differential ACPA Binding to Nuclear Antigens Reveals a PAD-Independent Pathway and a Distinct Subset of Acetylation Cross-Reactive Autoantibodies in Rheumatoid Arthritis.Frontiers in immunology · 2018Article
- Autoimmunity: Apoptotic cells induce immune memory.Nature reviews. Rheumatology · 2016Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Autoimmune diseases are characterized by pathogenic immune responses to self-antigens. In systemic lupus erythematosus (SLE), many self-antigens are found in apoptotic cells (ACs), and defects in removal of ACs from the body are linked to a risk for developing SLE. This includes pathological memory that gives rise to disease flares. In this study, we investigated how memory to AC-derived self-antigens develops and the contribution of self-memory to the development of lupus-related pathology. Multiple injections of ACs without adjuvant into wild-type mice induce a transient primary autoimmune response without apparent anti-nuclear Ab reactivity or kidney pathology. Interestingly, as the transient Ab response reached baseline, a single boost injection fully recalled the immune response to ACs, and this memory response was furthermore transferable into naive mice. Additionally, the memory response contains elements of pathogenicity, accompanied by selective memory to selective Ags. Thus, we provide evidence for a selective self-memory that underlies progression of the response to self-antigens with implications for SLE development therapy.
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