生物
CD8型
免疫学
人口
T细胞
细胞毒性T细胞
免疫系统
单核细胞
病毒学
医学
生物化学
环境卫生
体外
作者
Taylor Eddens,Olivia B. Parks,Dequan Lou,Li Fan,Jorna Sojati,Manda Jo Ramsey,Lori Schmitt,Cláudia Salgado,Miguel Reyes‐Múgica,Tim D. Oury,Craig A. Byersdorfer,Kong Chen,John Williams
标识
DOI:10.1101/2023.06.04.543430
摘要
Summary Respiratory viral infections remain a leading cause of morbidity and mortality. Using a murine model of human metapneumovirus (HMPV), we identified recruitment of a C1q-producing inflammatory monocyte population concomitant with viral clearance by adaptive immune cells. Genetic ablation of C1q led to reduced CD8 + T cell function. Production of C1q by a myeloid lineage was sufficient to enhance CD8 + T cell function. Activated and dividing CD8 + T cells expressed a putative C1q receptor, gC1qR. Perturbation of gC1qR signaling led to altered CD8 + T cell IFN-γ production and metabolic capacity. Autopsy specimens from fatal respiratory viral infections in children demonstrated diffuse production of C1q by an interstitial population. Humans with severe COVID-19 infection also demonstrated upregulation of gC1qR on activated and rapidly dividing CD8 + T cells. Collectively, these studies implicate C1q production from monocytes as a critical regulator of CD8 + T cell function following respiratory viral infection.
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