The Role of Tumor Necrosis Factor Receptor Superfamily Molecules on regulation of T cell response to Zika virus

The Role of Tumor Necrosis Factor Receptor Superfamily Molecules on regulation of T cell response to Zika virus
Research paper
Description: 

Zika virus (ZIKV) is a member of the Flaviviridae virus family and as of February 2016 has been declared a global public health emergency by the World Health Organization. Understanding the T cell response to ZIKV is critical in making steps towards developing vaccines and antiviral therapies. This project investigated the effect of tumor necrosis factor receptor (TNFR) superfamily members on T cell activation during a primary ZIKV infection. The T cell response was most aptly seen in wild-type C57BL/6J mice treated with an anti-Ifnar1 blocking antibody one day prior to infection. Expression levels of multiple TNFR superfamily members (BAFFR, CD30, ICOS, OX40, 4-1BB, CD27, GITR, and TNFR1) in both naïve and antigen specific T cells were analyzed over a variety of infection timepoints. In particular, expression levels of ICOS, GITR, and OX40 were higher in antigen-specific CD4+ and CD8+ T cells than naïve T cells at 5 days post infection. In terms of T cell kinetics of WT C57BL/6J mice treated with agonistic anti-OX40, anti-GITR, anti-OX40 and anti-GITR (combination), and isotype control antibody treatments 7 days post infection, there was a difference in the production of Granzyme B in antigen-specific CD8+ T cells in mice treated with agonistic anti-GITR and the combination agonistic anti-OX40 and anti-GITR antibody treatments. These findings warrant further study into the potential impact engaging OX40 and GITR could have on T cell response to ZIKV.

 

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WHDL ID: 
WHDL-00015206
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