AI Article Synopsis
- Respiratory viral infections are major health issues, and this study used a mouse model to explore how a specific inflammatory monocyte, producing C1q, aids in viral clearance by enhancing CD8 T cell activity.
- Genetic removal of C1q resulted in weaker CD8 T cell responses, while C1q from myeloid cells boosted their function, indicating a key role in immune response.
- In severe cases of respiratory infections like COVID-19, similar patterns of C1q and its receptor gC1qR were observed on activated CD8 T cells, highlighting the importance of C1q in regulating immune response during viral infections.
Article Abstract
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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10274684 | PMC |
| http://dx.doi.org/10.1101/2023.06.04.543430 | DOI Listing |
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