| Autor: |
Eddens T, Parks OB, Lou D, Fan L, Sojati J, Ramsey MJ, Schmitt L, Salgado CM, Reyes-Mugica M, Oury TD, Byersdorfer C, Chen K, Williams JV |
| Jazyk: |
angličtina |
| Zdroj: |
BioRxiv : the preprint server for biology [bioRxiv] 2023 Jun 06. Date of Electronic Publication: 2023 Jun 06. |
| DOI: |
10.1101/2023.06.04.543430 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
|
