Abstract
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.
Keywords: BTK; IRF7; SARS-CoV-2; TLR7; X-linked agammaglobulinemia; toll-like receptor 7.
【저자키워드】 SARS-CoV-2, TLR7, BTK, IRF7, X-linked agammaglobulinemia, toll-like receptor 7., 【초록키워드】 COVID-19, Chronic lymphocytic leukaemia, observations, interferons, TLR7, interferon, haematological malignancies, Toll-like receptor, dendritic cells, pDCs, Clinical course, plasmacytoid dendritic cells, type I interferons, CLL, inhibitor, patients, mechanism, agammaglobulinemia, IRF7, X-linked agammaglobulinemia, tyrosine, malignancies, Express, toll-like receptor 7, X-linked, combating, reduction in, patients with haematological, pDC, plasmacytoid dendritic cell, 【제목키워드】 COVID-19, Clinical course, reduced, contribute, plasmacytoid dendritic cell,