Evidence map›Paper›PMID 36361628›Full record

ArticleInternational journal of molecular sciences2022

Costimulatory CD226 Signaling Regulates Proliferation of Memory-like NK Cells in Healthy Individuals with Latent

Oscar Murillo, Josimar Dornelas Moreira, Weshely Kujur, Karen Velasco-Alzate, Sumit Sen Santara, Nagarjun V Konduru, Sachin Mulik

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

4 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Abnormal Elevation of the Expression of Costimulatory Molecule CD226 in Graves' DiseaseEndocrine, metabolic & immune disorders drug targets · 2026
    Article
  3. Review
  4. 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

7 authors at 2 institutions in 2 countries.

Oscar MurilloDepartment of Pulmonary Immunology, Center for Biomedical Research, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
Josimar Dornelas MoreiraDepartment of Pulmonary Immunology, Center for Biomedical Research, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
Weshely KujurDepartment of Pulmonary Immunology, Center for Biomedical Research, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
Karen Velasco-AlzateDepartment of Cellular and Molecular Biology, Center for Biomedical Research, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
Sumit Sen SantaraInfectious Diseases and Immunology Division, CSIR-Indian Institute of Chemical Biology, Kolkata 700032, West Bengal, India.
Nagarjun V KonduruDepartment of Cellular and Molecular Biology, Center for Biomedical Research, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
Sachin MulikDepartment of Pulmonary Immunology, Center for Biomedical Research, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
The University of Texas Health Science Center at Tyler · USIndian Institute of Chemical Biology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is now widely accepted that NK cells can acquire memory, and this makes them more effective to protect against some pathogens. Prior reports indicate memory-like NK cells (mlNKs) in murine model of Mycobacterium tuberculosis (Mtb) as well as in healthy individuals with latent TB infection (LTBI). The increased expression of CD226 was evident in mlNKs from LTBI+ people after stimulation with γ-irradiated Mtb (γ-Mtb). We thus evaluated the contribution of costimulatory CD226 signaling in the functionality of mlNKs in LTBI+ people. We found that blockade of CD226 signaling using the antibody- or CRISPR/Cas9-mediated deletion of the CD226 gene in NK cells diminished the proliferation of mlNKs from LTBI+ people. Blocking CD226 signaling also reduced the phosphorylation of FOXO1 and cMyc expression. Additionally, cMyc inhibition using a chemical inhibitor reduced proliferation by mlNKs from LTBI+ people. Moreover, blocking CD226 signaling reduced glycolysis in NK cells, and the inhibition of glycolysis led to reduced effector function of mlNKs from LTBI+ people. Overall, our results provide a role for CD226 signaling in mlNK responses to Mtb.

Indexed as

Latent TuberculosisMycobacterium tuberculosisAnimalsCell ProliferationHumansKiller Cells, NaturalMiceSignal TransductionCD226cMycFOXO1glycolysislatent TB infectionmemory-like NK cellsMycobacterium tuberculosis

Identifiers

PMID36361628
PMCPMC9653912
OpenAlexW4307555693

What OpenQuestion holds

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LicenceCC BY
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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.