Department of Laboratory Medicine, Translational Research Center Karolinska (TRACK), Stockholm, Sweden.
Department of Infectious Diseases, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Scand J Immunol. 2022 Apr;95(4):e13153. doi: 10.1111/sji.13153. Epub 2022 Mar 16.
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.
SARS-CoV-2 感染在血液系统恶性肿瘤患者中尤为严重，尤其是慢性淋巴细胞白血病（CLL）患者。基于一系列观察结果，我们提出 COVID-19 在 CLL 中侵袭性临床病程的潜在机制是这些患者中浆细胞样树突状细胞（pDC）的缺乏。事实上，pDC 表达 Toll 样受体 7（TLR7），与干扰素调节因子 7（IRF7）一起，使 pDC 能够产生大量的 I 型干扰素，这对于对抗 COVID-19 至关重要。用布鲁顿酪氨酸激酶（BTK）抑制剂治疗 CLL 可增加 pDC 的数量，可能是肿瘤负荷减少的继发作用。
