Evidence map›Paper›PMID 40780201›Full record

ReviewCell reports. Medicine2025

Host-intrinsic and host-extrinsic factors modulate immunity to Mtb infection, reinfection, and noncanonical vaccination routes.

Joshua D Bromley, Andrew W Simonson, Alex K Shalek, JoAnne L Flynn

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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

4 authors.

Joshua D BromleyRagon Institute of MGH, MIT, and Harvard, Cambridge, MA, USA; Institute for Medical Engineering and Science (IMES), Massachusetts Institute of Technology, Cambridge, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Andrew W SimonsonDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Center for Vaccine Research, University of Pittsburgh, Pittsburgh, PA, USA.
Alex K ShalekRagon Institute of MGH, MIT, and Harvard, Cambridge, MA, USA; Institute for Medical Engineering and Science (IMES), Massachusetts Institute of Technology, Cambridge, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA; Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA, USA; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
JoAnne L FlynnDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Center for Vaccine Research, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: joanne@pitt.edu.

Funding

IMMUNE MECHANISMS OF PROTECTION AGAINST MYCOBACTERIUM TUBERCULOSIS CENTER (IMPAC-TB)75N93019C00071 · NIAID · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI FORTUNE, SARAH · 2019 to 2025
$57.3M
Autoimmunity and Immunopathology Training ProgramT32AI089443 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SHLOMCHIK, MARK J · 2010 to 2024
$6.6M
IMMUNOLOGY AND INFECTIOUS DISEASES IN PUBLIC HEALTHT32AI007638 · NIAID · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI RUBIN, ERIC J. · 2000 to 2014
$2.2M
Gates Foundation INV-027498NIAID NIH HHS 75N93019C00071NIAID NIH HHS T32 AI007638NIAID NIH HHS T32 AI089443
6 · The paper itself

Abstract

Tuberculosis (TB) disease states and outcomes are highly heterogeneous. While this makes TB difficult to diagnose, monitor, and treat, it also presents opportunities to identify correlates of protection or disease severity that can be used as biomarkers and help inform future interventions. Immunological priming due to primary Mycobacterium tuberculosis (Mtb) infection can protect against subsequent reinfection; thus, comparing primary infection with reinfection can provide insights into features associated with host control. Here, we examine paradigms of natural and vaccine-induced immunity and examine how host-intrinsic and -extrinsic factors modulate the immune response to protect against infection and reinfection. We propose that the TB granuloma is a quasi-homeostatic system, building this model on findings from Mtb reinfection and successful prophylactics, which suggest that protective immunity depends on a balance of pro- and anti-inflammatory cellular phenotypes and that this balance can mitigate pathophysiological processes at the tissue and organismal level.

Indexed as

Host-Pathogen InteractionsMycobacterium tuberculosisReinfectionTuberculosisVaccinationAnimalsGranulomaHumansgranulomahomeostasisinflammationMtb reinfectionnatural immunity

Identifiers

PMID40780201
PMCPMC12432351

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.