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Immunological features of coronavirus disease 2019 in patients with cancer #MMPMID32977223
Thibaudin M; Fumet JD; Bon M; Hampe L; Limagne E; Ghiringhelli F
Eur J Cancer 2020[Nov]; 139 (ä): 70-80 PMID32977223show ga
BACKGROUND: Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2, has caused a major pandemic. Patients with cancer are at higher risk of severe COVID-19. We aimed to describe and compare the immunological features of cancer patients hospitalised for COVID-19 or other concomitant, cancer-related illness. METHODS: In this prospective study, the clinical and immunological characteristics of 11 cancer patients with COVID-19 and 11 non-COVID-19 cancer patients hospitalised in the same unit at the same period for other medical issues were analysed. We also used 10 healthy volunteers as controls. Peripheral immune parameters were analysed using multiparametric flow cytometry. RESULTS: The median age of COVID-19-positive cancer patients was 71.1 years, and 66.4 years for controls. Compared with non-COVID-19 cancer patients, COVID-19-positive cancer patients had more extensive lymphopenia and hypoalbuminemia, with higher levels of C-reactive protein. In COVID-19 patients, elevated procalcitonin was associated with a higher risk of death. By phenotypic analysis, COVID-19-positive patients presented CD3 lymphopenia, with inversion of the CD4/CD8 ratio and modification of monocyte activation, with accumulation of mMDSC (monocytic Myeloid-Derived Suppressor Cells) -like cells and a decrease in activated monocytes. Analysis of the T-cell compartment revealed a T-dependent inflammatory response with accumulation of Th17 cells and cytotoxic CD8 T cells producing TNFalpha, a decrease in HLA-DR (Human Leukocyte Antigen - DR isotype)-positive CD8 T cells and Treg/CD8 ratio. CONCLUSION: SARS-CoV-2 infection in cancer patients is associated with CD4 T-cell lymphopenia with induction of an inflammatory T-cell response, accumulation of IFNgamma(+) TNFalpha(+) CD8 T and Th17 cells, and a concomitant modification of monocyte activation status.