Mycobacterium tuberculosis-specific T cells restrain anti-cancer drug-induced neutrophilic lung inflammation in tuberculosis

Kee Woong Kwon, Tae Gun Kang, Jii Bum Lee, Eunsol Choi, Hagyu Kim, Min Chul Park, Sangwon Choi, Kyungmin Kim, Hyeong Woo Kim, Su Jin Jeong, Hye Ryun Kim, Sung Jae Shin () and Sang-Jun Ha ()
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Kee Woong Kwon: Gyeongsang National University
Tae Gun Kang: Yonsei University
Jii Bum Lee: Yonsei University College of Medicine
Eunsol Choi: Yonsei University College of Medicine
Hagyu Kim: Yonsei University College of Medicine
Min Chul Park: Yonsei University
Sangwon Choi: Yonsei University College of Medicine
Kyungmin Kim: Yonsei University College of Medicine
Hyeong Woo Kim: Gyeongsang National University
Su Jin Jeong: Yonsei University College of Medicine
Hye Ryun Kim: Yonsei University College of Medicine
Sung Jae Shin: Yonsei University College of Medicine
Sang-Jun Ha: Yonsei University

Nature Communications, 2025, vol. 16, issue 1, 1-20

Abstract: 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.

Date: 2025
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DOI: 10.1038/s41467-025-63930-0

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