Introduction

The immune responses of the host to respiratory infections in general and to rhinovirus infection in particular, are associated with upregulation of type I interferon (IFN) pathways (Bergauer et al., 2017b; a) in the airways and systemically in the blood cells {Hansel, 2017 #7;Hall, 1978 #4320}. Deficient systemic Interferon responses to respiratory infections have been observed in patients with non-controlled asthma {Sykes, 2014 #20;Bergauer, 2017 #10;Hentschke, 2017 #9;Isaacs, 1981 #4321}, suggesting that type I IFN could be used to improve lung function in asthma. IFN response of the host can be suppressed by infectious agents by upregulation of Programmed cell death protein 1 ligand (PD-L1) (Bergauer et al., 2017b; Bielor et al., 2017) which then inhibit T cell proliferation via binding to Programmed cell death protein 1 (PD1), considered as an immune checkpoint because it downregulates the immune responses (Ruibal et al., 2016).
To analyse the influence of rhinovirus on Interferon responses in asthma, we concentrated on the influence of human rhinovirus in the airways on Interferon induced PDL1 in the peripheral blood cells of children with and without asthma (Zhang et al., 2014; Liu et al., 2015).