Isolation and partial characterization of an ultraviolet-B induced suppressor factor which may be involved in Herpes Simplex Virus recrudescence

Cultured splenocytes from ultraviolet B (UVB) light irradiated mice release into supernatant fluid a soluble suppressor factor(s) (UVSF) that is not H-2 or antigen restricted. Normal splenocytes similarly released a suppressor factor (NSF) upon in vitro culture but its activity was markedly less than that of UVSF. Several aspects of T cell immunity were suppressed by UVSF and NSF. These included proliferative responses to phytoheraagglutinin (PHA) and pokeweed mitogen (PWM), the mixed lymphocyte reaction (MLR), cell-mediated lympholysis (CML), HSV-l-specific blastogenesis and cytotoxic T lymphocyte (CTL) induction. In each instance the activity of UVSF greatly exceeded that of NSF. The UVSF also inhibited proliferation of CTLL-2 cells, indicated that UVSF may interfere with IL-2 activity.

Results of titration curves in the above mentioned assays indicated that UVSF and NSF were not the same suppressive factors. Further support for this notion came from results of experiments designed to counteract the suppressive activity. Accordingly, either indomethacin or recombinant interleukin 2 (rIL-2) when added to MLR-NSF cultures could abrogate suppression when high concentrations of NSF were used (12.5%). However, when indomethacin or rIL-2 was added to MLR-UVSF cultures, suppression could be decreased but not abrogated even at very low concentrations of UVSF (0.39%). This further substantiates the idea that UVSF and NSF are not the same suppressive factors. The possible role of suppressor factors in regulating the T cell response to herpes simplex virus following viral reactivation from latency was discussed.