A Korean research team has identified the immunological mechanism by which anticancer drugs worsen tuberculosis in cancer patients. The findings are expected to provide basic data for establishing more effective and safer treatment strategies going forward.
Yonsei University Professors Ha Sang-jun of the College of Life Science and Biotechnology's Department of Biochemistry, Shin Sung-jae of the College of Medicine, Kim Hye-ryeon of the Department of Oncology, and Gwon Gi-ung of Gyeongsang National University College of Medicine said on the 16th that their team identified the pathological mechanism by which administering anticancer drugs exacerbates tuberculosis in the context of Mycobacterium tuberculosis infection. The study was published on the 6th (local time) in the international journal "Nature Communications."
Tuberculosis is one of the three major infectious diseases designated by the World Health Organization (WHO), along with acquired immunodeficiency syndrome (AIDS) and malaria, and is still regarded as the most serious infectious disease. It is estimated that about 2 billion people worldwide are infected with Mycobacterium tuberculosis, which is causing an enormous social and economic burden globally. In Korea, the incidence and prevalence of tuberculosis have been steadily declining compared with the past; however, as of 2024, the country still ranks among the highest in incidence and mortality from tuberculosis among member states of the Organisation for Economic Co-operation and Development (OECD).
As anticancer therapies have become more common in recent years, immune-related adverse events and cases of tuberculosis worsening have been reported in patients coinfected with Mycobacterium tuberculosis who are receiving anticancer drugs, but the immunopathogenic mechanism has not been clearly elucidated.
To address this, the team analyzed cancer patients who tested positive for Mycobacterium tuberculosis and visited Severance Hospital between 2005 and 2019 and confirmed that, in some patients, there was a sharp worsening of pulmonary tuberculosis along with "elevated neutrophils in the blood" after anticancer treatment.
To identify the cause of this clinical phenomenon, the researchers established an animal model of Mycobacterium tuberculosis infection and administered anticancer drugs. In the treatment group, they observed increased neutrophils in lung tissue, excessive inflammatory responses, and a rapid proliferation of Mycobacterium tuberculosis. They also found that in the treatment group, tuberculosis-specific T-cell responses, which are essential for controlling Mycobacterium tuberculosis, were markedly delayed.
The analysis showed that administering anticancer drugs suppresses the proliferation and activation of T cells that recognize and control Mycobacterium tuberculosis, while inducing excessive proliferation of neutrophil–monocyte progenitors in the bone marrow and their infiltration into lung tissue. This imbalance in immune cell composition triggered excessive inflammatory responses, promoting the pathological worsening of pulmonary tuberculosis.
Ha Sang-jun and Shin Sung-jae said, "By clarifying the mechanism underlying the correlation between anticancer drug use and the worsening of tuberculosis, this study is expected to contribute to establishing infection control guidelines for patients using anticancer drugs and to developing strategies to minimize side effects when administering anticancer drugs to patients with tuberculosis."
References
Nature Communications (2025), DOI: https://doi.org/10.1038/s41467-025-63930-0