IL-10 and PD-L1 operate through distinct pathways to suppress T-cell activity during persistent viral infection

DG Brooks, SJ Ha, H Elsaesser… - Proceedings of the …, 2008 - National Acad Sciences
DG Brooks, SJ Ha, H Elsaesser, AH Sharpe, GJ Freeman, MBA Oldstone
Proceedings of the National Academy of Sciences, 2008National Acad Sciences
Suppression of T-cell responses by host-derived regulatory factors is a key event leading to
viral persistence. Antibody blockade of either IL-10 or programmed death-ligand 1 (PD-L1)
during viral persistence enhances T-cell function and reduces viral titers. Because blockade
of these immunoregulatory networks represents a powerful approach to establish immune
control during persistent infection, it is important to determine whether these
immunoinhibitory factors act independently or jointly and if combined blockade of these …
Suppression of T-cell responses by host-derived regulatory factors is a key event leading to viral persistence. Antibody blockade of either IL-10 or programmed death-ligand 1 (PD-L1) during viral persistence enhances T-cell function and reduces viral titers. Because blockade of these immunoregulatory networks represents a powerful approach to establish immune control during persistent infection, it is important to determine whether these immunoinhibitory factors act independently or jointly and if combined blockade of these factors further enhances T-cell immunity and viral clearance. Herein, we demonstrate that the IL-10 and PD-L1 immunosuppressive pathways are mechanistically distinct. As a result, simultaneous blockade of IL-10 and PD-L1 was significantly more effective in restoring antiviral T-cell responses than blockade of either alone, and led to substantially enhanced control of an established persistent viral infection. Thus, combinatorial blockade of multiple immune-regulatory molecules may ultimately restore the T-cell responses required to tip the balance from viral persistence to immune-mediated control or elimination of persistent infection.
National Acad Sciences