CD4+ contrasuppressor T cells improve the resistance of thermally injured mice infected with HSV.

Modulation of burn-associated CD8+ CD11b+ T cell receptor gamma/delta+ suppressor T cells (BA2T cells) and improved resistance to herpesvirus infections was studied in thermally injured mice. The susceptibility of thermally injured mice to infection by herpes simplex virus (HSV) was approximately 100 times greater than it was in normal mice. The increased susceptibility of thermally injured mice to HSV infection was transferred to normal mice by BA2T cells, which appeared in spleens of mice 2-9 days after thermal injury. The suppressor cell activity of BA2T cells was effectively counteracted by CD4+ CD28+ T cell receptor alpha/beta+ Vicia villosa lectin adherent antisuppressor cells (designated as burn-induced contrasuppressor T cells; BCS cells), which were generated naturally in spleens of mice after the appearance of BA2T cells. The adoptive transfer of BCS cells to mice just after the injury improved the resistance of thermally injured mice to HSV infection to levels observed in normal mice. These results suggest that the increased susceptibility of thermally injured mice to HSV infection may be affected by BA2T suppressor cells and BCS cells may improve the resistance of thermally injured mice to HSV infection through the inhibition of BA2T suppressor cell activities.