Evidence map›Paper›PMID 40758870›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

Immune-responsive gene 1: The mitochondrial key to Th17 cell pathogenicity in CNS autoimmunity.

Mohammad Nematullah, Mena Fatma, Guoli Zhou, Bharat Prajapati, Faraz Rashid, Kameshwar Ayasolla, Mohammad Ejaz Ahmed, Ruicong She, Sajad Mir, Insha Zahoor and 3 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Immune-responsive gene 1: The mitochondrial key to Th17 cell pathogenicity in CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Mohammad NematullahDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.ORCID 0000-0001-8393-6717
Mena FatmaDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.
Guoli ZhouCenter for Statistical Training and Consulting, Michigan State University, East Lansing, MI 48824.ORCID 0000-0002-4497-5366
Bharat PrajapatiDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Västergötland 40530, Sweden.
Faraz RashidDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.
Kameshwar AyasollaDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.
Mohammad Ejaz AhmedDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.
Ruicong SheDepartment of Public Health Sciences, Henry Ford Health System, Detroit, MI 48202.
Sajad MirDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.
Insha ZahoorDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.ORCID 0000-0001-9919-1959
Nasrul HodaDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.
Ramandeep RattanDivision of Gynecology Oncology, Department of Women's Health Services, Henry Ford Hospital, Detroit, MI 48202.
Shailendra GiriDepartment of Neurology, Henry Ford Health System, Detroit, MI 48202.ORCID 0000-0002-7123-829X

Funding

Novel Regulation and Targeting of Macrophages Metabolism in Neuroinflammatory DisordersR01AI144004 · NIAID · HENRY FORD HEALTH SYSTEM · PI GIRI, SHAILENDRA · 2019 to 2023
$1.9M
Endogenous metabolite restricts GM-CSF signaling pathway in pathogenic macrophages to ameliorate CNS AutoimmunityR01NS112727 · NINDS · HENRY FORD HEALTH SYSTEM · PI GIRI, SHAILENDRA · 2019 to 2023
$1.6M
Henry Ford Hospital A10270 A30967HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI144004HHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS112727National Multiple Sclerosis Society (NMSS) RG-2111-38733NIAID NIH HHS R01 AI144004NINDS NIH HHS R01 NS112727
6 · The paper itself

Abstract

Pathogenic Th17 cells play crucial roles in CNS autoimmune diseases such as multiple sclerosis (MS), but their regulation by endogenous mechanisms remains unknown. Through RNA-seq analysis of primary brain glial cells, we identified immune-responsive gene 1 (

Indexed as

AutoimmunityCentral Nervous SystemEncephalomyelitis, Autoimmune, ExperimentalMitochondriaTh17 CellsAnimalsInterleukin-1betaMacrophagesMiceMice, Inbred C57BLMice, KnockoutMultiple SclerosisNLR Family, Pyrin Domain-Containing 3 ProteinSpinal CordInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseEAEIL1bIrg1scRNAseqTh17

Identifiers

PMID40758870
PMCPMC12358831

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.