Immune checkpoint inhibitor-related pneumonitis (ICI-P) during cancer treatment is rarely observed (<5%). ICI-P is more often observed in patients with nonsmall cell lung cancer (NSCLC) than in those with other cancers. Likewise, it is more common in those receiving programmed cell death (PD)-1/PD-1 ligand inhibitors rather than cytotoxic T-lymphocyte antigen (CTLA)-4 inhibitors alone. The frequency of ICI-P is higher when anti-PD-1 and anti-CTLA-4 are administered concomitantly. Despite the low fatality rate (≈13%), ICI-P is the leading cause of ICI-related deaths. This narrative review focuses on the epidemiology, clinical and radiological presentation and prognosis of ICI-P occurring in patients, especially those with advanced NSCLC. Emphasis is placed on the differences in terms of frequency or clinical picture observed depending on whether the ICI is used as monotherapy or in combination with another ICI or chemotherapy. Other pulmonary complications observed in cancer patients, yet not necessarily immune-related, are reviewed, such as sarcoid-like granulomatosis, tuberculosis or other infections. A proposal for pragmatic management, including differential diagnosis and therapeutic strategies, is presented, based on the ICI-P series reported in the literature and published guidelines.

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Medical explanations have often been thought on the model of biological ones and are frequently defined as mechanistic explanations of a biological dysfunction. In this paper, I argue that topological explanations, which have been described in ecology or in cognitive sciences, can also be found in medicine and I discuss the relationships between mechanistic and topological explanations in medicine, through the example of network medicine and medical genetics. Network medicine is a recent discipline that relies on the analysis of various disease networks (including diseasegene networks) in order to find organizing principles in disease explanation. My aim is to show how topological explanations in network medicine can help solving the conceptual issues that pure mechanistic explanations of the genetics of disease are currently facing, namely the crisis of the concept of genetic disease, the progressive geneticization of diseases and the dissolution of the distinction between monogenic and polygenic diseases. However, I will also argue that topological explanations should not be considered as independent and radically different from mechanistic explanations for at least two reasons. First, in network medicine, topological explanations depend on and use mechanistic information. Second, they leave out some missing gaps in disease explanation that require, in turn, the development of new mechanistic explanations. Finally, I will insist on the specific contribution of topological explanations in medicine: they push us to develop an explanation of disease in general, instead of focusing on single explanations of individual diseases. This last point may have major consequences for biomedical research.