Respiratory viral infections remain a leading cause of morbidity and mortality. Using a murine model of human metapneumovirus, 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. Autopsy specimens from fatal respiratory viral infections in children exhibited diffuse production of C1q by an interstitial population. Humans with severe coronavirus disease (COVID-19) infection also exhibited 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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| http://dx.doi.org/10.1165/rcmb.2024-0004OC | DOI Listing |
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