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Войти в исследования Nature genetics · 2023
Single-cell analyses and host genetics highlight the role of innate immune cells in COVID-19 severity.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Edahiro Ryuya, Shirai Yuya, Takeshima Yusuke, Sakakibara Shuhei, Yamaguchi Yuta, Murakami Teruaki, Morita Takayoshi, Kato Yasuhiro, Liu Yu-Chen, Motooka Daisuke, Naito Yoko, Takuwa Ayako, Sugihara Fuminori, Tanaka Kentaro, Wing James B, Sonehara Kyuto, Tomofuji Yoshihiko, Japan COVID-19 Task Force, Namkoong Ho, Tanaka Hiromu, Lee Ho, Fukunaga Koichi, Hirata Haruhiko, Takeda Yoshito, Okuzaki Daisuke, Kumanogoh Atsushi, Okada Yukinori
Аннотация
Mechanisms underpinning the dysfunctional immune response in severe acute respiratory syndrome coronavirus 2 infection are elusive. We analyzed single-cell transcriptomes and T and B cell receptors (BCR) of >895,000 peripheral blood mononuclear cells from 73 coronavirus disease 2019 (COVID-19) patients and 75 healthy controls of Japanese ancestry with host genetic data. COVID-19 patients showed a low fraction of nonclassical monocytes (ncMono). We report downregulated cell transitions from classical monocytes to ncMono in COVID-19 with reduced CXCL10 expression in ncMono in severe disease. Cell-cell communication analysis inferred decreased cellular interactions involving ncMono in severe COVID-19. Clonal expansions of BCR were evident in the plasmablasts of patients. Putative disease genes identified by COVID-19 genome-wide association study showed cell type-specific expressions in monocytes and dendritic cells. A COVID-19-associated risk variant at the IFNAR2 locus (rs13050728) had context-specific and monocyte-specific expression quantitative trait loci effects. Our study highlights biological and host genetic involvement of innate immune cells in COVID-19 severity.