Taylor Eddens, Olivia B Parks, Dequan Lou, Li Fan, Jorna Sojati, Manda Jo Ramsey, Lori Schmitt, Claudia M Salgado, Miguel Reyes-Mugica, Alysa Evans, Henry M Zou, Tim D Oury, Craig Byersdorfer, Kong Chen, John V Williams
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-expressing 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 necessary to enhance CD8+ T cell function. Activated and dividing CD8+ T cells expressed a C1q receptor, gC1qR. Perturbation of gC1qR signaling led to altered CD8+ T cell IFN-γ production, metabolic capacity, and cell proliferation...
May 2, 2024: American Journal of Respiratory Cell and Molecular Biology