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Single-cell multi-omics reveals dyssynchrony of the innate and adaptive immune system in progressive COVID-19 #MMPMID35064122
Unterman A; Sumida TS; Nouri N; Yan X; Zhao AY; Gasque V; Schupp JC; Asashima H; Liu Y; Cosme C Jr; Deng W; Chen M; Raredon MSB; Hoehn KB; Wang G; Wang Z; DeIuliis G; Ravindra NG; Li N; Castaldi C; Wong P; Fournier J; Bermejo S; Sharma L; Casanovas-Massana A; Vogels CBF; Wyllie AL; Grubaugh ND; Melillo A; Meng H; Stein Y; Minasyan M; Mohanty S; Ruff WE; Cohen I; Raddassi K; Niklason LE; Ko AI; Montgomery RR; Farhadian SF; Iwasaki A; Shaw AC; van Dijk D; Zhao H; Kleinstein SH; Hafler DA; Kaminski N; Dela Cruz CS
Nat Commun 2022[Jan]; 13 (1): 440 PMID35064122show ga
Dysregulated immune responses against the SARS-CoV-2 virus are instrumental in severe COVID-19. However, the immune signatures associated with immunopathology are poorly understood. Here we use multi-omics single-cell analysis to probe the dynamic immune responses in hospitalized patients with stable or progressive course of COVID-19, explore V(D)J repertoires, and assess the cellular effects of tocilizumab. Coordinated profiling of gene expression and cell lineage protein markers shows that S100A(hi)/HLA-DR(lo) classical monocytes and activated LAG-3(hi) T cells are hallmarks of progressive disease and highlights the abnormal MHC-II/LAG-3 interaction on myeloid and T cells, respectively. We also find skewed T cell receptor repertories in expanded effector CD8(+) clones, unmutated IGHG(+) B cell clones, and mutated B cell clones with stable somatic hypermutation frequency over time. In conclusion, our in-depth immune profiling reveals dyssynchrony of the innate and adaptive immune interaction in progressive COVID-19.