HIV infection causes numerical and functional defects of T and B cells and although antiretroviral therapy corrects many of these defects, some persist. The effects of immune activation mediated by the cytokine, interferon (IFN)-a, are implicated and were investigated here. IFN-a inhibited interleukin (IL)-7-mediated proliferation of T cells but this was not attributed to inhibition of the STAT5 signalling pathway that is induced by IL-7. IFN-a also inhibited IL-21-induced production of lgG antibodies by B cells via impairment of phosphorylation of STAT3. These findings confirm that IFN-a impacts upon key processes necessary for T and B cell recovery and function.
|Qualification||Doctor of Philosophy|
|Award date||22 Dec 2016|
|Publication status||Unpublished - 2016|