ReviewJournal of leukocyte biology2017
Taking the STING out of TLR-driven autoimmune diseases: good, bad, or indifferent?
Review in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 13 citations in OpenAlex.
- The cGAS-STING pathway: mechanistic basis, dual biological functions and translational therapeutic advances.Apoptosis : an international journal on programmed cell death · 2026Review
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
- Dual Targeting of TLR9 and cGAS-STING Pathways Attenuates Astrocyte Inflammatory Activation: Potential Implication in Multiple Sclerosis.Neurochemical research · 2025Article
- Herbal supplement Spirulina stimulates inflammatory cytokine production in patients with dermatomyositisiScience · 2023Article
- cGAS-STING Pathway Does Not Promote Autoimmunity in Murine Models of SLE.Frontiers in immunology · 2021Article
- USP38 Couples Histone Ubiquitination and Methylation via KDM5B to Resolve Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Wiskott-Aldrich syndrome protein restricts cGAS/STING activation by dsDNA immune complexes.JCI insight · 2020Article
- MAP kinase phosphatase-1, a gatekeeper of the acute innate immune response.Life sciences · 2020Review
- The many ways tissue phagocytes respond to dying cells.Immunological reviews · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Both endosomal and cytosolic-nucleic acid-sensing receptors can detect endogenous ligands and promote autoimmunity and autoinflammation. These responses involve a complex interplay among and between the cytosolic and endosomal sensors involving both hematopoietic and radioresistant cells. Cytosolic sensors directly promote inflammatory responses through the production of type I IFNs and proinflammatory cytokines. Inflammation-associated tissue damage can further promote autoimmune responses indirectly, as receptor-mediated internalization of the resulting cell debris can activate endosomal Toll-like receptors (TLR). Both endosomal and cytosolic receptors can also negatively regulate inflammatory responses. A better understanding of the factors and pathways that promote and constrain autoimmune diseases will have important implications for the development of agonists and antagonists that modulate these pathways.
Indexed as
Identifiers
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.