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Treatment of patients with non-small cell lung cancer (NSCLC) has been completely redesigned in the last years with the introduction of immune checkpoint blockade (ICB). Antiprogrammed cell death 1 (PD-1) or programmed death-ligand 1 (PD-L1) drugs are currently indicated worldwide for treatment of NSCLC.1 Known predictive positive biomarkers of response to these agents are PD-L1 expression and tumour mutational burden in tumour samples, but being the overall response rate is only 20%2 the identification of biomarker of resistance is desperately needed.
The only clinical feature that has represented a common exclusion criteria for all immunotherapy trials is the presence of concomitant diseases that require daily treatment with high-dose corticosteroids.1 However, patients with NSCLC often receive chronic treatment with a lower dose of corticosteroids, as part of best supportive care, for mitigating symptoms like dyspnoea or fatigue, or encephalic signs in the presence of brain metastasis.
Steroids are known to be immune-suppressive, by impairing T lymphocytes activation, by blocking the expansion of T helper 1 subgroup and favouring the T helper 2 one,3 by recruitment of T regulatory cells and promotion of M2 macrophage polarisation, and by affecting the microbiome.
Immunotherapy drugs are designed to reawake the cell-mediated side of the immune system to fight cancer; thus, immunotherapy needs an intact and functional immune …
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