Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells

Law, Helen KW; Cheung, Chung Yan; Sia, Sin Fun; Chan, Yuk On; Peiris, JS Malik; Lau, Yu Lung

Viruses may subvert the TLR response to evade the host defense by: (a) producting specific viral particles that block TLR function, (b) blocking TLR recognition and (c) stimulating viral replication through TLRs [23] . Viral infections, by RSV or influenza A, have been shown to upregulate TLR-3 and TLR-4 expression in host airway epithelial cells, leading to increased signalling activity and proinflammatory cytokine production [23] . More recently, TLR-4 was shown to be upregulated in mice with acid-induced or inactivated avian influenza-induced lung injuries; and TLR-4 deficient mice showed less severe acute lung injuries to these challenges [24] . We, therefore, determined if SARS-CoV may modulate the TLRs expression on DCs. In this study, there was no induction nor suppression of TLRs in SARS-CoV infected DCs (Figs. 1 &2) . The variations between samples were high, but the expression levels of some extracellular TLRs (TLR-1, TLR-2, TLR-4, TLR-5) and some intracellular TLRs (TLR-7, TLR-8) in CB DCs were higher than that in adult DCs (Table 1 ). Further investigation is needed to determine if the expression is responsible for the slightly higher Type I inferferon expression reported in CB DCs [8] and to identify any correlation with less severe SARS in children.