Do reduced numbers of plasmacytoid dendritic cells contribute to the aggressive clinical course of COVID-19 in chronic lymphocytic leukaemia?
Carl Inge Edvard SmithRula ZainAnders ÖsterborgMarzia PalmaMarcus BuggertPeter BergmanYenan BrycesonPublished in: Scandinavian journal of immunology (2022)
Infections with SARS-CoV-2 have been unduly severe in patients with haematological malignancies, in particular in those with chronic lymphocytic leukaemia (CLL). Based on a series of observations, we propose that an underlying mechanism for the aggressive clinical course of COVID-19 in CLL is a paucity of plasmacytoid dendritic cells (pDCs) in these patients. Indeed, pDCs express Toll-like receptor 7 (TLR7), which together with interferon-regulatory factor 7 (IRF7), enables pDCs to produce large amounts of type I interferons, essential for combating COVID-19. Treatment of CLL with Bruton's tyrosine kinase (BTK) inhibitors increased the number of pDCs, likely secondarily to the reduction in the tumour burden.
Keyphrases
- dendritic cells
- sars cov
- toll like receptor
- tyrosine kinase
- immune response
- coronavirus disease
- regulatory t cells
- respiratory syndrome coronavirus
- inflammatory response
- nuclear factor
- epidermal growth factor receptor
- chronic lymphocytic leukemia
- end stage renal disease
- ejection fraction
- newly diagnosed
- chronic kidney disease
- prognostic factors
- early onset
- risk factors
- replacement therapy