Evidence map›Paper›PMID 39435656›Full record

ArticleJCI insight2024

Immune exhaustion in ME/CFS and long COVID.

Natalie Eaton-Fitch, Penny Rudd, Teagan Er, Livia Hool, Lara Herrero, Sonya Marshall-Gradisnik

Abstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
–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

34 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Cellular Metabolic Signatures of Long COVID-19.Infectious disease reports · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  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

6 authors.

Natalie Eaton-FitchNational Centre for Neuroimmunology and Emerging Diseases.
Penny RuddInstitute for Biomedicine and Glycomics, Griffith University, Gold Coast, Australia.
Teagan ErSchool of Human Sciences (Physiology), The University of Western Australia, Perth, Australia.
Livia HoolSchool of Human Sciences (Physiology), The University of Western Australia, Perth, Australia.
Lara HerreroInstitute for Biomedicine and Glycomics, Griffith University, Gold Coast, Australia.
Sonya Marshall-GradisnikNational Centre for Neuroimmunology and Emerging Diseases.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and long COVID are debilitating multisystemic conditions sharing similarities in immune dysregulation and cellular signaling pathways contributing to the pathophysiology. In this study, immune exhaustion gene expression was investigated in participants with ME/CFS or long COVID concurrently. RNA was extracted from peripheral blood mononuclear cells isolated from participants with ME/CFS (n = 14), participants with long COVID (n = 15), and healthy controls (n = 18). Participants with ME/CFS were included according to Canadian Consensus Criteria. Participants with long COVID were eligible according to the case definition for "Post COVID-19 Condition" published by the World Health Organization. RNA was analyzed using the NanoString nCounter Immune Exhaustion gene expression panel. Differential gene expression analysis in ME/CFS revealed downregulated IFN signaling and immunoglobulin genes, and this suggested a state of immune suppression. Pathway analysis implicated dysregulated macrophage activation, cytokine production, and immunodeficiency signaling. Long COVID samples exhibited dysregulated expression of genes regarding antigen presentation, cytokine signaling, and immune activation. Differentially expressed genes were associated with antigen presentation, B cell development, macrophage activation, and cytokine signaling. This investigation elucidates the intricate role of both adaptive and innate immune dysregulation underlying ME/CFS and long COVID, emphasizing the potential importance of immune exhaustion in disease progression.

Indexed as

COVID-19Fatigue Syndrome, ChronicSARS-CoV-2AdultAgedCase-Control StudiesCytokinesFemaleHumansImmune System ExhaustionLeukocytes, MononuclearMaleMiddle AgedPost-Acute COVID-19 SyndromeSignal TransductionCytokinesAdaptive immunityImmunologyInnate immunity

Identifiers

PMID39435656
PMCPMC11529985

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.