Evidence map›Paper›PMID 28031336›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

Autophagy in Dendritic Cells and B Cells Is Critical for the Inflammatory State of TLR7-Mediated Autoimmunity.

Chi G Weindel, Lauren J Richey, Abhiruchi J Mehta, Mansi Shah, Brigitte T Huber

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 14% of its field
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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  8. Autophagy pathways in autoimmune diseases.Journal of autoimmunity · 2023
    Review
  9. Article
  10. Review
  11. Cell type-specific mechanistic target of rapamycin-dependent distortion of autophagy pathways in lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022
    Review
  12. The "Self-Sacrifice" of ImmuneCells in Sepsis.Frontiers in immunology · 2022
    Review
  13. Review
  14. Autophagy in major human diseases.The EMBO journal · 2021
    Review
  15. Review
  16. Article
  17. Review
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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

5 authors at 1 institution in 1 country.

Chi G WeindelProgram in Genetics, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111.
Lauren J RicheyDivision of Laboratory Animal Medicine, Tufts University, Boston, MA 02111; and.
Abhiruchi J MehtaDepartment of Integrative Physiology and Pathobiology, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111.
Mansi ShahDepartment of Integrative Physiology and Pathobiology, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111.
Brigitte T HuberProgram in Genetics, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111; Brigitte.huber@tufts.edu.ORCID 0000-0001-5090-791X
Tufts University · US

Funding

Tufts Clinical and Translational Research InstituteUL1TR001064 · NCATS · TUFTS UNIVERSITY BOSTON · PI SELKER, HARRY P. · 2013 to 2017
$26.4M
NCATS NIH HHS UL1 TR001064
6 · The paper itself

Abstract

Individuals suffering from autoimmune disorders possess a hyperactive cellular phenotype where tolerance to self-antigens is lost. Autophagy has been implicated in both the induction and prevention of autoimmunity, and modulators of this cellular recycling process hold high potential for the treatment of autoimmune diseases. In this study, we determine the effects of a loss of autophagy in dendritic cells (DCs), as well as both B cells and DCs, in a TLR7-mediated model of autoimmunity, similar to systemic lupus erythematosus, where both cell types are critical for disease. Although a loss of DC autophagy slowed disease, the combined loss of autophagy in both cell types resulted in a lethal sepsis-like environment, which included tissue inflammation and hyperproduction of inflammasome-associated cytokines. Ablation of B cell signaling reversed this phenotype, indicating that activation of these cells is an essential step in disease induction. Thus, autophagy plays a dichotomous role in this model of disease.

Indexed as

AutoimmunityAnimalsAutophagyB-LymphocytesDendritic CellsInflammationInterleukin-18Lupus Erythematosus, SystemicLymphadenopathyMembrane GlycoproteinsMiceMice, Inbred C57BLSplenomegalyToll-Like Receptor 7Interleukin-18Membrane GlycoproteinsTlr7 protein, mouseToll-Like Receptor 7

Identifiers

PMID28031336
PMCPMC5263064
OpenAlexW2566962221

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.