Host–pathogen
PD-1 blockade reactivates TB via TNF
Open access · cc by · source: Europe PMC
Anti-PD-1 immunotherapy can reactivate tuberculosis through TNF-α dysregulation.
Study at a glance
- Design
- Other — Human TB lung PD-1+ T-cell profiling plus infection models of anti-PD-1 effects
- N
- N=35 · 35 patients with medically indicated lung resection; matched blood for 23; animal/in-vitro models secondary
- Population
- Patients undergoing lung resection for TB or sequelae (plus infection models)
- Outcome
- PD-1 expression and TNF-dependent effects of PD-1 blockade in TB
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
PD-1 is present on tissue-resident T cells in TB lung (35 patients); TNF-α is primarily responsible and neutralization reverses the anti-PD-1 phenotype.
Methodology
Profiled PD-1+ T cells in resected human TB lung, then used infection models to test anti-PD-1 effects and TNF neutralization.
Limitations
Not a randomized oncology trial endpoint paper; focuses on host–pathogen mechanism.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Multiple empirical papers in this library examine host–pathogen with mechanistic biological findings.
Evidence for the claim as stated.
PD-1 is present on tissue-resident T cells in TB lung (35 patients); TNF-α is primarily responsible and neutralization reverses the anti-PD-1 phenotype.
Evidence for the claim as stated.
Systems and scales differ across host–pathogen studies (species, tissues, methods), so mechanisms should not be over-generalised.
Evidence for the claim as stated.
In resected human TB lung from 35 patients, PD-1 marked tissue-resident T cells; infection models then showed that TNF-α is primarily responsible for anti-PD-1–driven reactivation and that TNF neutralization reverses the phenotype. Tissue IF here is a human spatial observation paired with mechanistic models, not a randomized oncology endpoint trial.
Evidence for the claim as stated.
IF is a screening camera in Vero cells (berzosertib 100 nM, 48 hpi), a tissue census in TB lung (35 patients), a trafficking assay for Smo/Rab5/spike, and a polarity assay in enteroids. 'Positive staining' in a drug screen is not the same claim as PD-1 on human tissue-resident T cells or as K140/K165 moving Rab5 off endosomes.
Evidence for the claim as stated.
PD-1 staining on tissue-resident T cells in resected TB lung (35 patients) was paired with infection models in which TNF-α drove anti-PD-1 reactivation and TNF neutralization reversed the phenotype. Cytometry or related IF/flow phenotyping here is a host-cell census, not a randomized oncology trial endpoint.
Evidence for the claim as stated.
Flow is counting different objects. Salmonella work counts persistent bacteria inside LN DCs (50–1,000, lumen clear at 3 h); hESC work counts CXCR4+ DE-like cells under 1.5% O2; TB work profiles PD-1+ T cells in 35 human lungs. Those gates are not one 'immune panel'.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Systems and scales differ across host–pathogen studies (species, tissues, methods), so mechanisms should not be over-generalised.
IF is a screening camera in Vero cells (berzosertib 100 nM, 48 hpi), a tissue census in TB lung (35 patients), a trafficking assay for Smo/Rab5/spike, and a polarity assay in enteroids. 'Positive staining' in a drug screen is not the same claim as PD-1 on human tissue-resident T cells or as K140/K165 moving Rab5 off endosomes.
- Supports · ATR inhibitor blocks SARS-CoV-2
- Supports · How does monoubiquitin turn down Rab5?
- Supports · Apical-out enteroids for pathogen access
Flow is counting different objects. Salmonella work counts persistent bacteria inside LN DCs (50–1,000, lumen clear at 3 h); hESC work counts CXCR4+ DE-like cells under 1.5% O2; TB work profiles PD-1+ T cells in 35 human lungs. Those gates are not one 'immune panel'.
Related papers in this topic
Same topic cluster — not a recommendation engine.