ArticleNature communications2025
Mycobacterium tuberculosis-specific T cells restrain anti-cancer drug-induced neutrophilic lung inflammation in tuberculosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed.
- Neutrophils and tuberculosis - insights into immunobiology and pathogenesis.Molecular biology reports · 2026Review
- An ESAT-6-convergent prime-boost vaccination combining recombinant BCG expressing Mycobacterium marinum ESX-1 and ESAT-6/GLA-SE improves TB protection.NPJ vaccines · 2026Article
- Exploring Host-driven Immunopathological Factors Developing Severe Tuberculosis: Insights from Comparative Mouse Models.International journal of biological sciences · 2026Article
- Reprogramming the host: Mycobacterium tuberculosis as a silent architect of the immuno-tumoral.Frontiers in cellular and infection microbiology · 2025Review
- The significance of trained immunity in cancer.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Cancers are a risk factor for active tuberculosis (TB), and anti-cancer drugs can independently cause TB progression. To understand the underlying mechanisms, mice infected with Mycobacterium tuberculosis (Mtb) were treated with gemcitabine (Gem), cisplatin, or paclitaxel. These treatments delay Mtb-specific T cell responses, increase bacterial loads, and cause hyperinflammation with permissive neutrophils in the lungs. However, depleting Mtb-permissive neutrophils reduce bacterial levels and G-CSF production, thereby attenuating lung immunopathology. Additionally, Mtb-specific T cell responses generated by BCG vaccination inhibit bacterial growth and neutrophil infiltration even after Gem treatment. Gem induces granulocyte-biased generation in the bone marrow via G-CSF signaling, which led to lung neutrophil inflammation. However, pre-existing Mtb-specific T cell responses from BCG vaccination normalizes granulopoiesis by restricting G-CSF production. These findings show the mechanism of anti-cancer drug-induced neutrophilic lung inflammation in TB and highlight the role of Mtb-specific T cell responses in maintaining balanced hematopoiesis against Gem-induced TB immunopathogenesis.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.