Evidence map›Paper›PMID 26432899›Full record

ReviewJournal of immunology (Baltimore, Md. : 1950)2015

Nucleic Acid-Sensing Receptors: Rheostats of Autoimmunity and Autoinflammation.

Shruti Sharma, Katharine A Fitzgerald, Michael P Cancro, Ann Marshak-Rothstein

Abstract readReview
In one paragraph

Review in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed.

  1. Trial
  2. Nucleotide metabolism, leukodystrophies, and CNS pathology.Journal of inherited metabolic disease · 2024
    Review
  3. Article
  4. The roles of ABCB1/P-glycoprotein drug transporters in regulating gut microbes and inflammation: insights from animal models, old and new.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. The balance between gasdermin D and STING signaling shapes the severity of schistosome immunopathology.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Shruti SharmaProgram in Innate Immunity, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605; and.
Katharine A FitzgeraldProgram in Innate Immunity, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605; and.
Michael P CancroDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.
Ann Marshak-RothsteinProgram in Innate Immunity, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605; and ann.rothstein@umassmed.edu.

Funding

Toll-Like Receptors in Systemic Autoimmune DiseaseP01AR050256 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SHLOMCHIK, MARK J · 2004 to 2013
$13.4M
Distinct Functional Outcomes of BCR/TLR7 and BCR/TLR9 Co-engagementR01AR066808 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MARSHAK-ROTHSTEIN, ANN · 2015 to 2019
$2.6M
NIAMS NIH HHS AR050256NIAMS NIH HHS P01 AR050256NIAMS NIH HHS R01 AR066808
6 · The paper itself

Abstract

Distinct families of germline-encoded pattern recognition receptors can sense both microbial and endogenous nucleic acids. These DNA and RNA sensors include endosomal TLRs and cytosolic sensors upstream of stimulator of type I IFN genes (STING) and MAVS. The existence of overlapping specificities for both foreign and self nucleic acids suggests that, under optimal conditions, the activity of these receptors is finely tuned to effectively mediate host defense yet constrain pathogenic self-reactivity. This equilibrium becomes disrupted with the loss of either TLR9 or STING. To maintain immune protection, this loss can be counterbalanced by the elevated response of an alternative receptor(s). Unfortunately, this adjustment can lead to an increased risk for the development of systemic autoimmunity, as evidenced by the exacerbated clinical disease manifestations of TLR9-deficient and STING-deficient autoimmune-prone mice. These studies underscore the delicate balance normally maintained by tonic signals that prevent unchecked immune responses to nucleic acids released during infections and cellular duress or death.

Indexed as

AnimalsAutoimmune DiseasesDNAHumansMembrane ProteinsMiceRNASTING ProteinToll-Like Receptor 9DNAMembrane ProteinsRNASTING1 protein, humanSTING ProteinTLR9 protein, humanToll-Like Receptor 9

Identifiers

PMID26432899
PMCPMC4593056

What OpenQuestion holds

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Registered trials

None linked

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.