ArticleImmunologic research2013
TLR7 drives accumulation of ABCs and autoantibody production in autoimmune-prone mice.
Article in Immunologic research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 93 citations in OpenAlex.
- The Developmental and Functional Implications of Age-Associated B Cells (ABCs) Across Tissue Microenvironments.Immunological reviews · 2026Review
- Female mice with a Xist deletion in B cells can develop lupus-associated phenotypes.Cell reports · 2026Article
- Multiomic Immune Profiling of Pediatric Transplant Recipients Identifies Cell States Associated with Vaccine Response.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- IFNγ-induced IRF1 synergizes with TLR7 signals to tune the IRF4-IRF8 axis and drive pathogenic effector B cell fate.bioRxiv : the preprint server for biology · 2026Article
- The multilayered identity of B cell memory.Cellular & molecular immunology · 2026Review
- TLR7 and TLR9 have overlapping but distinct roles in systemic lupus erythematosus and Sjögren's disease.Frontiers in immunology · 2026Review
- Aging and vaccines: impact of immunosenescence and inflammaging in vaccine response.Frontiers in aging · 2026Review
- Age-associated B-cells across the rheumatoid arthritis continuum: from early immunopathogenesis to comorbidities.Frontiers in aging · 2026Review
- Deletion of Ptpn2 in B cells promotes autoimmunity via TLR and JAK/STAT signaling.JCI insight · 2025Article
- CD21 primes extrafollicular differentiation of autoreactive B cells in a TLR7-driven lupus model.Science immunology · 2025Article
- IL-4 alters TLR7-induced B cell developmental program in lupus.Clinical immunology (Orlando, Fla.) · 2025Article
- The Inactive X Chromosome: A Genetic Driver of Female-Biased Rheumatic Autoimmune Disorders?European journal of immunology · 2025Review
- Innate Immune Receptors as Dynamic Modulators of Extrafollicular Autoimmune B Cell Response.Immunological reviews · 2025Review
- Age-Associated B Cells in Autoimmune Diseases: Pathogenesis and Clinical Implications.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
- TLR7 activation of age-associated B cells mediates disease in a mouse model of primary Sjögren's disease.Journal of leukocyte biology · 2024Article
- Lupus-associated innate receptors drive extrafollicular evolution of autoreactive B cells.bioRxiv : the preprint server for biology · 2024Article
- Mechanisms and consequences of sex differences in immune responses.Nature reviews. Nephrology · 2024Review
- Tlr7 drives sex- and tissue-dependent effects in Sjögren's disease.Frontiers in cell and developmental biology · 2024Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Although autoantibodies are the hallmarks of most autoimmune diseases, the mechanisms by which autoreactive B cells are generated and accumulate are still poorly understood. Overexpression of Toll-like receptor 7 (TLR7) that recognizes single-stranded RNAs has been implicated in systemic lupus erythematosus (SLE), although the cellular mechanism by which this receptor drives the disease is unknown. We recently identified a population of CD11c(+) age-associated B cells (ABCs) which is driven by TLR7 signaling, secretes autoantibodies and appears in autoimmune-prone mice by the time of onset of autoimmunity. Mice lacking the Mer receptor develop autoantibodies and splenomegaly similar to other mouse models of SLE. Here, we show that Mer(-/-) mice that lack TLR7 fail to develop anti-chromatin IgG antibodies, perhaps because they also fail to develop ABCs. Moreover, depletion of CD11c(+) ABCs from Mer(-/-) mice leads to rapid reduction in autoantibodies. Together, these data strongly suggest that ABCs and/or their descendants are the primary source of autoantibodies in Mer(-/-) mice and that TLR7 signaling is crucial for accumulation of ABCs and development of autoantibodies. These data demonstrate for the first time that TLR7, and not TLR9, is responsible for generation of anti-chromatin IgG antibodies in Mer(-/-) mice.
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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.