Abstract
BackgroundRespiratory infections, in general, and rhinovirus infection specifically are the main reason for asthma exacerbation in children and programmed cell death protein 1 ligand (PD‐L1) expression inhibits T cell responses.ObjectiveCould the interferon (IFN) type I expression in peripheral blood mononuclear cells (PBMCs) improve disease exacerbation in pediatric asthma?ResultsHere we found increased level of PD‐L1 messenger RNA (mRNA) in total blood cells isolated from preschool children with virus‐induced asthma, with lower percentage of forced expiratory volume in 1 second and with high serum levels of the C‐reactive‐protein.Conclusions and Clinical RelevanceThese data indicate that, in the presence of infection in the airways of preschool children, worse asthma is associated with induced PD‐L1 mRNA expression in blood cells. Further, type I IFN, IFN‐β, a cytokine that is involved in the clearance of infections, was found to be associated with a better lung function in asthmatic children. These data suggest that improving peripheral blood IFN type I expression in PBMCs in pediatric asthma could improve disease exacerbation due to suppressing PD‐L1 expression in blood cells.
Highlights
Respiratory infections, in general, and rhinovirus infection are the main reason for asthma exacerbation in children and programmed cell death protein 1 ligand (PD‐L1) expression inhibits T cell responses
We recently described that acute in vitro infection of peripheral blood mononuclear cells (PBMCs) from preschool children with and without asthma with RV, a single‐stranded RNA picornavirus, is associated with the upregulation of IFN‐regulated genes like STAT1, STAT2, and IFN regulatory factor 1.1,2 paradoxically, IFNγ upregulates PD‐L1, a factor involved in silencing/ exhausting of activated T cells by ligating PD1 on the surface of T cells.[10]
We found that increased PD‐L1 messenger RNA (mRNA) expression correlated with reduced forced expiratory volume in 1 second (FEV1)% and peak expiratory flow (PEF)% (Figure 1H), indicating that asthmatic preschool children with RV colonization in the airways have worse respiratory function associated with PD‐L1 induction in their PBMCs
Summary
Asthma,[1,2,4,5] suggesting that type I IFN could be used to improve lung function in asthma. The immune responses of the host to respiratory infections, can be suppressed by infectious agents by upregulation of in general, and to rhinovirus (RV) infection in particular, are programmed cell death protein 1 ligand (PD‐L1),[2,6] which associated with upregulation of type I interferon (IFN) pathways[1,2] in the airways and systemically in the blood cells.[3] Deficient systemic IFN responses to respiratory infections have been observed in patients with noncontrolled inhibit T cell proliferation via binding to programmed cell death protein 1 (PD1), considered as an immune checkpoint because it downregulates the immune responses.[7]. To analyze the influence of RV on IFN responses in asthma, we concentrated on the influence of human RV in the airways on IFN‐induced PD‐L1 in the peripheral blood cells of children with and without asthma.[8,9]
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