Pulmonary toxicity of immune checkpoint immunotherapy

Pulmonary toxicity of immune checkpoint immunotherapy

2024 | Mohammad I. Ghanbar' and Karthik Suresh
The article reviews the pulmonary toxicity associated with immune checkpoint inhibitors (ICIs) in the context of non-small cell lung cancer (NSCLC). ICIs, while improving patient outcomes, can cause immune-related adverse events (irAEs), particularly checkpoint inhibitor pneumonitis (CIP), which is a significant concern due to its high morbidity and mortality rates. The review covers the epidemiology and clinical characteristics of CIP, as well as emerging research on its pathobiology. It highlights the complex interplay between the immune system and cancer, emphasizing the role of immune checkpoints such as CTLA-4 and PD-1 in regulating T cell activity. The article discusses the mechanisms underlying CIP, including increased T cell activity, clonal T cell selection, upregulated autoantibodies, and cytokine dysfunction. Genetic predisposition and the gut microbiome are also explored as potential factors contributing to CIP. The review concludes by emphasizing the need for further research to better understand the pathogenesis of CIP and to develop effective treatment strategies.The article reviews the pulmonary toxicity associated with immune checkpoint inhibitors (ICIs) in the context of non-small cell lung cancer (NSCLC). ICIs, while improving patient outcomes, can cause immune-related adverse events (irAEs), particularly checkpoint inhibitor pneumonitis (CIP), which is a significant concern due to its high morbidity and mortality rates. The review covers the epidemiology and clinical characteristics of CIP, as well as emerging research on its pathobiology. It highlights the complex interplay between the immune system and cancer, emphasizing the role of immune checkpoints such as CTLA-4 and PD-1 in regulating T cell activity. The article discusses the mechanisms underlying CIP, including increased T cell activity, clonal T cell selection, upregulated autoantibodies, and cytokine dysfunction. Genetic predisposition and the gut microbiome are also explored as potential factors contributing to CIP. The review concludes by emphasizing the need for further research to better understand the pathogenesis of CIP and to develop effective treatment strategies.
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