ReviewImmunology and cell biology2016
Germinal centers and autoimmune disease in humans and mice.
Review in Immunology and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- Exploring the role of APRIL in autoimmunity: implications for therapeutic targeting in systemic lupus erythematosus, rheumatoid arthritis, and Sjögren's syndrome.Frontiers in immunology · 2025Review
- Cutting Edge: Low-dose Recombinant IL-2 Treatment Prevents Autoantibody Responses in Systemic Lupus Erythematosus via Regulatory T Cell-independent Depletion of T Follicular Helper Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Optimized Protocols forFrontiers in immunology · 2022Article
- Artemisinin analogue SM934 protects against lupus-associated antiphospholipid syndrome via activation of Nrf2 and its targets.Science China. Life sciences · 2021Article
- Monoallelic IRF5 deficiency in B cells prevents murine lupus.JCI insight · 2021Article
- The Imbalance of Circulating Follicular T Helper Cell Subsets in Primary Sjögren's Syndrome Associates With Serological Alterations and Abnormal B-Cell Distribution.Frontiers in immunology · 2021Article
- Review
- Multi-omics: Differential expression of IFN-γ results in distinctive mechanistic features linking chronic inflammation, gut dysbiosis, and autoimmune diseases.Journal of autoimmunity · 2020Article
- B cell memory: building two walls of protection against pathogens.Nature reviews. Immunology · 2020Review
- Spatial and functional heterogeneity of follicular helper T cells in autoimmunity.Current opinion in immunology · 2019Review
- BAFF inhibition in SLE-Is tolerance restored?Immunological reviews · 2019Review
- Critical role of Interleukin 21 and T follicular helper cells in hypertension and vascular dysfunction.JCI insight · 2019Article
- Emerging immunotherapies for autoimmune kidney disease.Human vaccines & immunotherapeutics · 2019Review
- Poly- and autoreactivity of HIV-1 bNAbs: implications for vaccine design.Retrovirology · 2018Review
- Toll-like receptors in lupus nephritis.Journal of biomedical science · 2018Review
- B Cell Receptor and CD40 Signaling Are Rewired for Synergistic Induction of the c-Myc Transcription Factor in Germinal Center B Cells.Immunity · 2018Article
- Targeting the programmed cell death-1 pathway in rheumatoid arthritis.Autoimmunity reviews · 2017Review
- Chronic airway inflammation provides a unique environment for B cell activation and antibody production.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017Article
- Novel aspects of autoimmunity.Immunology and cell biology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Antibodies are involved in the pathogenesis of many autoimmune diseases. Although the mechanisms underlying the antibody response to infection or vaccination are reasonably well understood, we still have a poor understanding of the nature of autoimmune antibody responses. The most well studied are the anti-nuclear antibody responses characteristic of systemic lupus erythematosus and studies over the past decade or so have demonstrated a critical role for signaling by TLR7 and/or TLR9 in B cells to promote these responses. These Toll-like receptors (TLRs) can promote T-cell-independent extrafollicular antibody responses with a heavy-chain class switch and a low degree of somatic mutation, but they can also strongly boost the germinal center response that gives rise to high-affinity antibodies and long-lived plasma cells. TLRs have been shown to enhance affinity maturation in germinal center responses to produce high-affinity neutralizing antibodies in several virus infection models of mice. Although more data are needed, it appears that anti-nuclear antibodies in mouse models of lupus and in lupus patients can be generated by either pathway, provided there are genetic susceptibility alleles that compromise B-cell tolerance at one or another stage. Limited data in other autoimmune diseases suggest that the germinal center response may be the predominant pathway leading to autoantibodies in those diseases. A better understanding of the mechanisms of autoantibody production may ultimately be helpful in the development of targeted therapeutics for lupus or other autoimmune diseases.
Indexed as
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What OpenQuestion holds
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.