Abstract: | Intravenous infection with Theiler's virus strain GD VII causes acute encephalomyelitis in mice. Endogenous IFN-γ produced in the spinal cord is important to protect the tissue in mice infected with this virus. Neither CD4+ cells nor CD8+ cells infiltrated the spinal cords of infected mice until Day 9 postinfection. However, the number of CD3+/TCR-γδ+ cells increased in the spinal cords of mice infected with the virus. These cells resided in the spinal cords of normal mice, and produced IFN-γ as a result of stimulation by immobilized anti-CD3 mAb. Elimination of CD3+ cells by the administration of a specific mAb augmented viral replication and suppressed production of endogenous IFN-γ. Depletion of TCR-αβ+ cells and ASGM1+ cells did not affect the viral replication, and did not alter the production of IFN-γ. Therefore, CD3+/TCR-αβ– cells producing IFN-γ play an important role in the protection of the spinal cord against Theiler's virus infection. These results suggest that CD3+/TCR-αβ– cells might be identical to TCR-γδ+ cells. |