Smoking and SARS-CoV-2 impair Dendritic Cells and regulate DC-SIGN expression in Tissues
Supplemental tables of the publication "Smoking and SARS-CoV-2 impair Dendritic Cells and regulate DC-SIGN expression in Tissues" Cai et al., 2020. Table S1. Mendelian Randomization inferred causal effect of plasma expression of ACE2, DC-SIGN and L-SIGN on COVID-19 risk and severity in the European population. Table S2. The top 100 CD209 expression associated traits identified by GWAS. Table S3. The top 100 CD209 lung expression associated traits identified by PheWAS. Table S4. Mendelian Randomization inferred causal effect of plasma expression of DC-SIGN on cell count and percentage. Smoking and SARS-CoV-2 impair Dendritic Cells and regulate DC-SIGN expression in Tissues Guoshuai Cai*, Yohan Bossé, Mulong Du, Helmut Albrecht, Fei Qin, Xuanxuan Yu, Xizhi Luo, Michelle Androulakis, Xia Zhu, Jun Zhou, Xiang Cui, Changhua Yi, Chao Cheng, Mitzi Nagarkatti, Prakash Nagarkatti, David Christiani, Michael Whitfield, Christopher Amos, Feifei Xiao* The current spreading novel coronavirus SARS-CoV-2 is highly infectious and pathogenic. In this study, we screened the gene expression of these three receptors (ACE2, DC-SIGN and L-SIGN) and DC status in bulk and single cell transcriptomic datasets of upper airway, lung or blood of smokers, non-smokers and COVID-19 patients. We found smoking increased DC-SIGN gene expression and inhibited DC maturation and its ability of T cell stimulation. In COVID-19, DC-SIGN gene expression was interestingly decreased in lung DCs but increased in blood DCs. Strikingly, DCs shifted from cDCs to pDCs in COVID-19, but the shift was trapped in an immature stage (CD22+ or ANXA1+ DC) with MHCII downregulation in severe cases. This observation indicates that DCs in severe cases may stimulate innate immune responses but fail to specifically recognize SARS-CoV-2. Our study provides insights into smoking effect on COVID-19 risk and the profound modulation of DC function in severe COVID-19.