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).