Hong Kong Med J 2012;18(Suppl 3):S28-30
Role of dendritic cells in SARS coronavirus infection
YL Lau, JSM Peiris, HKW Law
Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Hong Kong
1. Severe acute respiratory syndrome coronavirus (SARS-CoV) entered and replicated in monocyte-derived dendritic cells (DCs), but virus replication was incomplete. In addition, SARS-CoV did not induce apoptosis or maturation of infected DCs.
2. SARS-CoV infected DCs showed low expression of antiviral cytokines (IFN-_, IFN-_, IFN-_, and IL-12p40), moderate up-regulation of proinflammatory cytokines (TNF-_ and IL-6), and significant up-regulation of inflammatory chemokines (MIP-1_, RANTES, IP-10, and MCP-1).
3. SARS-CoV did not modulate gene expression of Toll-like receptors (TLR-1 to 10) but induced significant up-regulation of chemokine receptors (CCR-1, CCR-3, CCR-5).
4. SARS-CoV induced high expression of TRAIL but not FasL gene expression in DCs.
5. The characteristic phenotype of SARS-CoV infected DCs suggested some possible mechanisms of immune escape and amplification of immunopathology in SARS.
2. SARS-CoV infected DCs showed low expression of antiviral cytokines (IFN-_, IFN-_, IFN-_, and IL-12p40), moderate up-regulation of proinflammatory cytokines (TNF-_ and IL-6), and significant up-regulation of inflammatory chemokines (MIP-1_, RANTES, IP-10, and MCP-1).
3. SARS-CoV did not modulate gene expression of Toll-like receptors (TLR-1 to 10) but induced significant up-regulation of chemokine receptors (CCR-1, CCR-3, CCR-5).
4. SARS-CoV induced high expression of TRAIL but not FasL gene expression in DCs.
5. The characteristic phenotype of SARS-CoV infected DCs suggested some possible mechanisms of immune escape and amplification of immunopathology in SARS.