Speaker: Dr. Lishan Su

Topic:    HIV-induced pDC/IFN-I signaling in immune exhaustion and AIDS: A novel axis of evil in inflammatory diseases?

Time:     13:30-15:00, April. 26th (Thursday)

Venue:   D326, Medical Science Building

Host:      Dr. Chen Dong  

Abstract

Plasmacytoid dendritic cells (pDC) are the major type I interferon (IFN-I) producing cells and play important roles in antiviral immune responses during acute virus infection. However, sustained pDC activation and IFN-I induction has been correlated with disease progression in chronic virus infection.

We have recently functionally defined the HIV-pDC-IFN axis in HIV-1 immunopathogenesis, and studied the mechanisms of pDC/IFN-induced immune suppression, and its role in HIV reservoir persistence. We have discovered that blocking the pDC/INF-I axis during HIV infection reverses all HIV-related diseases even in the presence of higher levels of HIV replication. We further show that low levels of pDC/IFN-I signaling contribute to the immune dysfunction and foster HIV-1 persistence in cART-treated hosts. Transient depletion of pDC or blocking IFNAR during suppressive ART has been shown to provide a novel strategy to enhance immune recovery and to control HIV-1 reservoirs. Our findings thus not only functionally reveal the role of pDC/IFN-I in HIV-1 and other inflammatory diseases, the IFNAR blocking and pDC-depleting mAb will also be developed into novel therapeutics to enhance immune recovery to treat HIV-associated diseases and cancers.