PD-1 blockade reactivates TB via TNF
Anti-PD-1 immunotherapy can reactivate tuberculosis through TNF-α dysregulation.
Source
Anti-PD-1 immunotherapy leads to tuberculosis reactivation via dysregulation of TNF-α
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
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PD-1 blockade reactivates TB via TNF
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Thirty-five patients with lung resection.
In thirty-five patients undergoing medically indicated lung resection to treat TB or TB sequalae, PD-1 expression was measured on T cells isolated from the lung and matched blood samples, available for 23 patients, by flow cytometry.
Human cohort?
In thirty-five patients undergoing medically indicated lung resection
What they did
Profiled PD-1+ T cells in resected human TB lung, then used infection models to test anti-PD-1 effects and TNF neutralization.
What they found
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.
The limits
What it doesn't show
Not a randomized oncology trial endpoint paper; focuses on host–pathogen mechanism.
Key terms
- PD-1
- Inhibitory checkpoint receptor on T cells.
- TNF-α
- Inflammatory cytokine central to TB control/pathology.
- Reactivation
- Return of active TB from controlled infection.
- Granuloma
- Structured immune aggregate containing Mtb.
- Checkpoint blockade
- Antibody therapy blocking PD-1/PD-L1.
- Tissue-resident T cell
- CD69/CD103-marked lung T cell.
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Patients n:
Common questions
Human lung n?
Thirty-five patients.
Key cytokine?
TNF-α.
Rescue?
TNF neutralization reverses phenotype.
Topic?
Host–pathogen immunology.
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