Evidence map›Paper›PMID 40906796›Full record

ArticlePLoS pathogens2025

Mycobacterium tuberculosis impairs protective cytokine production via transcription factor MafB manipulation.

Hiroyuki Saiga, Masaki Ueno, Toshiki Tamura, Yusuke Tsujimura, Masamitsu N Asaka, Yumiko Tsukamoto, Tetsu Mukai, Michito Hamada, Satoru Takahashi, Takashi Tanaka and 4 more

Abstract read
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In one paragraph

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

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Hiroyuki SaigaDepartment of Immunology, Faculty of Medicine, Kagawa University, Kagawa, Japan.ORCID 0000-0001-9189-4043
Masaki UenoDepartment of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Toshiki TamuraLeprosy Research Center, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.
Yusuke TsujimuraLeprosy Research Center, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.
Masamitsu N AsakaLeprosy Research Center, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.
Yumiko TsukamotoLeprosy Research Center, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.
Tetsu MukaiLeprosy Research Center, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.
Michito HamadaDepartment of Anatomy and Embryology, Institute of Medicine, University of Tsukuba, Ibaraki, Japan.
Satoru TakahashiDepartment of Anatomy and Embryology, Institute of Medicine, University of Tsukuba, Ibaraki, Japan.
Takashi TanakaLaboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences (IMS), Kanagawa, Japan.
Tsuneyasu KaishoIndustry-Government-Academia Collaboration Promotion Headquarters, Wakayama Medical University, Wakayama, Japan.
Yoshimasa TakahashiResearch Center for Vaccine Development, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.
Katsuaki HoshinoDepartment of Immunology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Manabu AtoLeprosy Research Center, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.

Funding

JSPS KAKENHIKagawa University Research Promotion ProgramTakeda Science Foundation
6 · The paper itself

Abstract

Although an increased expression of the transcription factor v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB) has been reported in patients with active tuberculosis (TB), its potential role in Mycobacterium tuberculosis infection remains unknown. Herein, we report that MafB in macrophages is a regulator of the pro-inflammatory cytokines, TNF-α and IL-12p40, which are crucial for host defense against M. tuberculosis infection. Cell-based luciferase assays showed that MafB inhibited TNF-α and IL-12p40 transcriptional activity in a dose-dependent manner. At the molecular level, MafB interacted with IFN regulatory factor (IRF)-5 and PU.1 and inhibited IRF-5- and PU.1-mediated transactivation, via the basic-leucine zipper domain. Analysis using gene-deficient macrophages demonstrated that the suppressed pro-inflammatory cytokine production during M. tuberculosis infection depends on MafB expression. Finally, in vivo studies indicated that M. tuberculosis-mediated increase of MafB expression was responsible for the exacerbation of M. tuberculosis infection. Thus, our results provide a functional view of MafB as a cytokine regulator as well as novel insights into host factors involved in TB susceptibility.

Indexed as

CytokinesMafB Transcription FactorMycobacterium tuberculosisTuberculosisAnimalsHumansInterferon Regulatory FactorsInterleukin-12 Subunit p40MacrophagesMiceMice, Inbred C57BLMice, KnockoutTrans-ActivatorsTumor Necrosis Factor-alphaCytokinesInterferon Regulatory FactorsInterleukin-12 Subunit p40MAFB protein, humanMafb protein, mouseMafB Transcription FactorTrans-ActivatorsTumor Necrosis Factor-alpha

Identifiers

PMID40906796
PMCPMC12419584

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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 OpenQuestion graph.