Evidence map›Paper›PMID 30226884›Full record

ArticlePloS one2018

CLEC16A regulates splenocyte and NK cell function in part through MEK signaling.

Rahul Pandey, Marina Bakay, Heather S Hain, Bryan Strenkowski, Barakat Z B Elsaqa, Jeffrey D Roizen, Jake A Kushner, Jordan S Orange, Hakon Hakonarson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Is DEXI a Multiple Sclerosis Susceptibility Gene?International journal of molecular sciences · 2025
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  4. International journal of molecular sciences · 2023
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  11. Article
  12. The Genetic Contribution to Type 1 Diabetes.Current diabetes reports · 2019
    Review
  13. Article
  14. The Autoimmune Disorder Susceptibility GeneFrontiers in immunology · 2019
    Article
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

9 authors at 3 institutions in 2 countries.

Rahul PandeyThe Center for Applied Genomics, The Children's Hospital of Philadelphia, Philadelphia, PA, United States of America.
Marina BakayThe Center for Applied Genomics, The Children's Hospital of Philadelphia, Philadelphia, PA, United States of America.
Heather S HainThe Center for Applied Genomics, The Children's Hospital of Philadelphia, Philadelphia, PA, United States of America.ORCID 0000-0003-1139-2882
Bryan StrenkowskiThe Center for Applied Genomics, The Children's Hospital of Philadelphia, Philadelphia, PA, United States of America.
Barakat Z B ElsaqaDepartment of Medicine, Jordan University of Science and Technology, Irbid, Jordan.
Jeffrey D RoizenDivision of Endocrinology and Diabetes Children's Hospital of Philadelphia, Philadelphia, PA, United States of America.ORCID 0000-0002-3384-6200
Jake A KushnerSection of Pediatric Diabetes and Endocrinology, Department of Pediatric Medicine, Endocrine-Metabolism, Texas Children's Hospital, Houston, TX, United States of America.
Jordan S OrangeSection of Immunology, Allergy, and Rheumatology, Department of Pediatric Medicine, Texas Children's Hospital, Houston, TX, United States of America.
Hakon HakonarsonThe Center for Applied Genomics, The Children's Hospital of Philadelphia, Philadelphia, PA, United States of America.ORCID 0000-0003-2814-7461
Children's Hospital of Philadelphia · USTexas Children's Hospital · USJordan University of Science and Technology · JO

Funding

Fine Mapping and Functional Evaluation of Selected Type 1 Diabetes LociDP3DK085708 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI HAKONARSON, HAKON, POLYCHRONAKOS, CONSTANTIN · 2009 to 2009
$4.8M
NIDDK NIH HHS DP3 DK085708
6 · The paper itself

Abstract

CLEC16A is implicated in multiple autoimmune diseases. We generated Clec16a inducible knockout (KO) mice to examine the functional link between CLEC16A auto-inflammation and autoimmunity. Clec16a KO mice exhibited weight loss and thymic and splenic atrophy. Mitochondrial potential was lowered in KO mice splenocytes resulting in aggregation of unhealthy mitochondria in B, T, and NK cells. In Clec16a KO mice we detected disrupted mitophagy in splenic B and T cells. NK cells from Clec16a KO mice exhibited increased cytotoxicity. Incomplete mitophagy was attenuated with PI3K and/or MEK inhibition in Clec16a KO mice. Our results demonstrate a functional link between CLEC16A and disrupted mitophagy in immune cells and show that incomplete mitophagy predisposes the KO mice to inflammation. Taken together, loss of function variants in CLEC16A that are associated with decreased CLEC16A expression levels may contribute to inflammation in autoimmunity through disrupted mitophagy. Drugs modulating mitophagy reverse the process and may be effective in treating and preventing autoimmunity in individuals with risk associated CLEC16A variants.

Indexed as

MAP Kinase Signaling SystemAnimalsBlotting, WesternCytokinesEnzyme-Linked Immunosorbent AssayFlow CytometryKiller Cells, NaturalLectins, C-TypeMembrane Potential, MitochondrialMiceMice, KnockoutMitophagyMonosaccharide Transport ProteinsSpleenCLEC16A protein, mouseCytokinesLectins, C-TypeMonosaccharide Transport Proteins

Identifiers

PMID30226884
PMCPMC6143231
OpenAlexW2890730650

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.