Evidence map›Paper›PMID 41370123›Full record

ArticleCell reports2025

ESAT-6 and CFP-10 reactive IgG in patients with tuberculosis inhibits intracellular bacteria.

Joshua R Miles, Pei Lu, Shuangyi Bai, Genesis P Aguillón-Durán, Javier E Rodríguez-Herrera, Bronwyn M Gunn, Blanca I Restrepo, Lenette L Lu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

8 authors.

Joshua R MilesDepartment of Immunology, UT Southwestern Medical Center, Dallas, TX, USA.
Pei LuDivision of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA.
Shuangyi BaiPaul G. Allen School of Global Health, College of Veterinary Medicine, Washington State University, Pullman, WA, USA.
Genesis P Aguillón-DuránDepartment of Epidemiology, School of Public Health, University of Texas Health Science Center at Houston, Brownsville Campus, Brownsville, TX, USA.
Javier E Rodríguez-HerreraDepartamento Estatal de Micobacteriosis, Secretaría de Salud de Tamaulipas, Reynosa 88630, Matamoros 87370, Tamaulipas, México.
Bronwyn M GunnPaul G. Allen School of Global Health, College of Veterinary Medicine, Washington State University, Pullman, WA, USA.
Blanca I RestrepoDepartment of Epidemiology, School of Public Health, University of Texas Health Science Center at Houston, Brownsville Campus, Brownsville, TX, USA; School of Medicine, South Texas Diabetes and Obesity Institute, University of Texas Rio Grande Valley, Edinburg, TX, USA; I.CARE and Population Health, Texas Biomedical Research Institute, San Antonio, TX, USA.
Lenette L LuDepartment of Immunology, UT Southwestern Medical Center, Dallas, TX, USA; Division of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA; Parkland Health, Dallas, TX, USA. Electronic address: lenette.lu@utsouthwestern.edu.

Funding

INTEGRATIVE IMMUNOLOGY TRAINING PROGRAMT32AI005284 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Nan Yan · 2003 to 2026
$7.4M
Defining the antibody interface between Mycobacterium tuberculosis and host immunityR01AI158858 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI LU, LENETTE · 2021 to 2025
$2.1M
Role of metabolic Me-macrophages in the pathogenesis of tuberculosis during diabetesR21AI144541 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI JAGANNATH, CHINNASWAMY, RESTREPO, BLANCA I · 2020 to 2021
$443k
NIAID NIH HHS R01 AI158858NIAID NIH HHS R21 AI144541NIAID NIH HHS T32 AI005284
6 · The paper itself

Abstract

Perspectives beyond the CD4 T cell interferon (IFN)-γ paradigm are needed to understand immunity in tuberculosis (TB). Growing data in patients across a spectrum of TB highlight that changes in antibody Fc domain glycosylation and Fc effector functions correlate with disease and impact Mycobacterium tuberculosis (Mtb) infection. How antigen-specific antibodies within polyclonal responses affect bacteria is less clear. This study examines antibodies targeting ESAT-6 and CFP-10, Mtb virulence proteins essential for pathogenesis. Data from patients with TB show that polyclonal immunoglobulin (Ig)G reactive to ESAT-6 and CFP-10 diverges from other Mtb and non-Mtb antigens with enhanced sialylation, afucosylation, natural killer cell-mediated cellular cytotoxicity, and association with anti-microbial activity against intracellular Mtb. Monoclonal antibody studies show that intracellular Mtb inhibition is dependent on antigen binding, N-linked glycans, and Fc-Fc receptor (FcR) engagement. These findings demonstrate that some antibodies in patients inhibit Mtb in its quintessential intracellular niche, opening avenues to appreciate how humoral immunity impacts TB.

Indexed as

Antibodies, BacterialAntigens, BacterialBacterial ProteinsImmunoglobulin GMycobacterium tuberculosisTuberculosisFemaleGlycosylationHumansMaleMiddle AgedAntibodies, BacterialAntigens, BacterialBacterial ProteinsCFP-10 protein, Mycobacterium tuberculosisESAT-6 protein, Mycobacterium tuberculosisImmunoglobulin Gantibodyantibody glycosylationCP: immunologyCP: microbiologyFc effector functionsmacrophageMycobacterium tuberculosistuberculosis

Identifiers

PMID41370123
PMCPMC12842600

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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.