2009
DOI: 10.1186/1471-2172-10-35
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Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells

Abstract: Background: The SARS outbreak in 2003 provides a unique opportunity for the study of human responses to a novel virus. We have previously reported that dendritic cells (DCs) might be involved in the immune escape mechanisms for SARS-CoV. In this study, we focussed on the gene expression of toll-like receptors (TLRs), chemokine receptors (CCRs) and death receptor ligands in SARS-CoV infected DCs. We also compared adult and cord blood (CB) DCs to find a possible explanation for the age-dependent severity of SARS. Show more

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Cited by 47 publications
(49 citation statements)
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“…The inverse correlation among the levels of the proapoptotic TRAIL and the counts of CD4+ and CD8+ T lymphocyte subpopulations supports the hypothesis that TRAIL is related to lymphocytic cell death. A similar phenomenon has been reported in patients infected with HIV [Cummins and Badley, ], respiratory syncytial virus [Roe et al, ], SARS coronavirus [Law et al, ], measles virus [Okada et al, ], and in primate models of Ebola virus disease [Hensley et al, ]. Therefore, apoptosis might be a contributing factor that modulates the number of lymphocytes in dengue infection, as documented previously [Myint et al, ].…”
Section: Discussionsupporting
confidence: 80%
“…The inverse correlation among the levels of the proapoptotic TRAIL and the counts of CD4+ and CD8+ T lymphocyte subpopulations supports the hypothesis that TRAIL is related to lymphocytic cell death. A similar phenomenon has been reported in patients infected with HIV [Cummins and Badley, ], respiratory syncytial virus [Roe et al, ], SARS coronavirus [Law et al, ], measles virus [Okada et al, ], and in primate models of Ebola virus disease [Hensley et al, ]. Therefore, apoptosis might be a contributing factor that modulates the number of lymphocytes in dengue infection, as documented previously [Myint et al, ].…”
Section: Discussionsupporting
confidence: 80%
“…Although the consequences of the timing of these signals are not yet understood, SARS-CoV infection of susceptible aged mice leads to elevated levels of proinflammatory cytokines with ARDS association, including TNFa, IL-6, and IL-1b [30,31]. Chemokine receptors CCR1, CCR2, and CCR5 have protective roles during MA15-SARS-CoV infection in the mouse model as well as SARS-CoV infection of human DCs, indicating the importance of cell recruitment in controlling SARS-CoV infections [51,53]. Transcriptional profiles of ISGs associated with increased SARS-CoV disease have been described in several model systems, but the consequences of ISG signaling responses to SARS-CoV infection has not been characterized [23 ,31,40 ,41 ,50 ].…”
Section: Cytokines Chemokines and Isgsmentioning
confidence: 99%
“…SARS-CoV also infects human MØs and DCs, but viral replication is abortive and no infectious virus particles are produced Law et al, 2005;Tseng et al, 2005;Yilla et al, 2005;Ziegler et al, 2005). Despite the lack of productive infection in human MØs, SARS-CoV induced the expression of proinflammatory chemokines, including CXCL-10 and CCL-2 but, in contrast, antiviral cytokines such as IFN-α and INF-β were basically absent Law et al, 2005Law et al, , 2009Tseng et al, 2005). In unproductive infections of DCs, SARS-CoV induced CXCL-10, CCL-2, CCL-3, CCL-5, and CXCL-10 " CXCL-10 " CXCL-10 # Apoptosis CCL-2, -36, -5 " CCL-5…”
Section: Interaction Of Cov Vaccine Candidates With Cells Of the Immumentioning
confidence: 99%