ArticleiScience2022
DOCK8-expressing T follicular helper cells newly generated beyond self-organized criticality cause systemic lupus erythematosus.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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.
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Who cites it
8 citing papers in PubMed.
- Regulation of follicular helper T cell subset differentiation in health and disease.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Comprehensive Profiling of T- and B-Cell Receptor Repertoires Demonstrates Impaired Developmental and Activation of Adaptive Immunity in DOCK8 Deficiency.Journal of clinical immunology · 2026Article
- Dock8 regulates Th2 cell differentiation through ANXA1.Fundamental research · 2026Article
- The Role of m6A Modification in the Development of Systemic Lupus Erythematosus via the TGF-β Signaling Pathway.Journal of immunology research · 2026Review
- Review
- Clinical outcomes of baricitinib in patients with systemic lupus erythematosus: Pooled analysis of SLE-BRAVE-I and SLE-BRAVE-II trials.PloS one · 2025Article
- Help me help you: emerging concepts in T follicular helper cell differentiation, identity, and function.Current opinion in immunology · 2024Review
- SARS-CoV-2-The Role of Natural Immunity: A Narrative Review.Journal of clinical medicine · 2022Review
Corrections and comments
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Authors and funding
27 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathogens including autoantigens all failed to induce systemic lupus erythematosus (SLE). We, instead, studied the integrity of host's immune response that recognized pathogen. By stimulating TCR with an antigen repeatedly to levels that surpass host's steady-state response, self-organized criticality, SLE was induced in mice normally not prone to autoimmunity, wherein T follicular helper (Tfh) cells expressing the guanine nucleotide exchange factor DOCK8 on the cell surface were newly generated. DOCK8
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Registered trials
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