Pulmonary endothelium-derived PD-L1 induced by the H9N2 avian influenza virus inhibits the immune response of T cells

PD-L1 0301 basic medicine Tumor Necrosis Factor-alpha H9N2 virus Research T-Lymphocytes Endothelial Cells Infectious and parasitic diseases RC109-216 Virus Replication B7-H1 Antigen Rats Specific Pathogen-Free Organisms Up-Regulation 3. Good health Interferon-gamma 03 medical and health sciences Primary microvascular endothelial cells T cell immune response Microvessels Influenza A Virus, H9N2 Subtype Animals Lung Cells, Cultured
DOI: 10.1186/s12985-020-01341-x Publication Date: 2020-07-06T09:03:53Z
ABSTRACT
The PD-1/PD-L1 pathway is an inhibitory signaling that maintains the balance between immune response and immunotolerance, its overactivation in cancer viral infections inhibits T cell function. target cells of various viruses, microvascular endothelial (MECs) have been shown to be key regulatory points regulation virion diffusion vivo during infection with multiple influenza virus subtypes. Furthermore, avian (AIV) can induce immunosuppression by causing imbalances responses organ damage. Thus, aim this study was investigate whether H9N2 inhibited function migrated across MECs upregulating PD-L1 expression on MECs. susceptibility rat pulmonary (RPMECs) evaluated a plaque-forming assay immunofluorescence staining. Then, we quantified mRNA protein levels RPMECs induced using quantitative real-time PCR flow cytometry. interaction activated infected revealed coculture system. effect endothelial-derived investigated ELISA cytometry or without PD-L1-specific antibody. Surface staining showed replicated RPMECs. Both level were upregulated virus. virus-induced significantly reduced secretions IL-2, IFN-γ granzyme B perforin cells. above data increased after treatment anti-PD-L1 antibody, confirming mentioned findings. In addition, induction decreased proliferative capacity cocultured but did not affect apoptosis rate Taken together, results suggest able inhibit
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