Evidence map›Paper›PMID 41204075›Full record

ArticleBMC immunology2025

A quadral biosignature of IFN-γ, IL-2, IL-12 and IP-10 increases the diagnostic potential for latent tuberculosis among diabetic patients in Uganda.

Phillip Ssekamatte, Diana Sitenda, Rose Nabatanzi, Marjorie Nakibuule, Davis Kibirige, Andrew Peter Kyazze, David Patrick Kateete, Bernard Ssentalo Bagaya, Obondo James Sande, Reinout van Crevel and 2 more

Abstract read
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Article in BMC immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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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

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No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

12 authors.

Phillip SsekamatteDepartment of Immunology and Molecular Biology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda. psekamate@gmail.com.
Diana SitendaDepartment of Immunology and Molecular Biology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda.
Rose NabatanziDepartment of Immunology and Molecular Biology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda.
Marjorie NakibuuleMedical Research Council/Uganda Virus Research Institute and London School of Hygiene & Tropical Medicine Uganda Research Unit, Entebbe, Uganda.
Davis KibirigeDepartment of Medicine, Uganda Martyrs Hospital Lubaga, Kampala, Uganda.
Andrew Peter KyazzeDepartment of Internal Medicine, School of Medicine, College of Health Sciences, Makerere University, Kampala, Uganda.
David Patrick KateeteDepartment of Immunology and Molecular Biology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda.
Bernard Ssentalo BagayaDepartment of Immunology and Molecular Biology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda.
Obondo James SandeDepartment of Immunology and Molecular Biology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda.
Reinout van CrevelDepartment of Internal Medicine and Radboud Centre for Infectious Diseases, Radboud University Medical Centre, Nijmegen, the Netherlands.
Stephen CoseMedical Research Council/Uganda Virus Research Institute and London School of Hygiene & Tropical Medicine Uganda Research Unit, Entebbe, Uganda.
Irene Andia BiraroMedical Research Council/Uganda Virus Research Institute and London School of Hygiene & Tropical Medicine Uganda Research Unit, Entebbe, Uganda.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 2 diabetes mellitus (DM) increases both the risk of acquiring latent tuberculosis (TB) infection (LTBI) and progression to active TB. The immunological mechanisms underlying the increased susceptibility remain poorly understood. This study aimed to elucidate the impact of DM on Mtb-specific cytokine and chemokine responses and identify potential biomarkers for LTBI regardless of DM status.

methodsThis cross-sectional study recruited 164 participants with LTBI-DM (n = 51), LTBI-only (n = 63), DM-only (n = 12) and healthy controls (n = 38) at Kiruddu National Referral Hospital. Cytokine and chemokine responses were measured in ESAT-6 and CFP-10 whole blood stimulated supernatants using the Luminex assay. Linear regression with age as a covariate and false discovery rate (p < 0.050) correction were performed on log

resultsLTBI-DM was associated with decreased Mtb-specific IFN-γ (p

conclusionDiabetes mellitus impairs Th1, inflammatory, and regulatory cytokine and chemokine responses during LTBI. A multivariate biosignature of IFN-γ, IL-2, IL-12 and IP-10 outperforms single-marker assays (e.g., variability in IFN-γ due to immunosuppression in DM) and offers robust identification of LTBI regardless of DM status, highlighting the additive value of combining mediators that capture distinct immunological axes. The improved biosignature specificity may minimise false positives in DM populations, who often exhibit comorbidities that could mimic LTBI-associated inflammation. Our findings support validating combined biomarker approaches to enhance LTBI diagnosis and prognosis in the immunocompromised DM population.

Indexed as

Diabetes Mellitus, Type 2Latent TuberculosisMycobacterium tuberculosisAdultBiomarkersChemokine CXCL10Cross-Sectional StudiesFemaleHumansInterferon-gammaInterleukin-12Interleukin-2MaleMiddle AgedUgandaBiomarkersChemokine CXCL10CXCL10 protein, humanInterferon-gammaInterleukin-12Interleukin-2BiomarkersChemokinesCytokinesDiabetes mellitusLatent tuberculosis infectionMycobacterium tuberculosis

Identifiers

PMID41204075
PMCPMC12595789

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.