Treatment of encephalomyocarditis virus-induced central nervous system demyelination with monoclonal anti-T-cell antibodies.

AUTOR(ES)

Sriram, S

RESUMO

Infection of BALB/c mice with the M variant of encephalomyocarditis virus resulted in the development of a paralytic syndrome in 7 to 10 days. The paralysis was maximal during the period of viral clearance; most of the animals recovered from the initial deficit and showed no delayed recurrences. Pathologically, the white matter of brain and spinal cord showed well-demarcated areas of perivascular cuffing, demyelination, and, during recovery, remyelination by oligodendrocytes--all suggestive of postinfectious encephalomyelitis. Depletion of either the CD4 or CD8 subset of T cells in vivo with the appropriate monoclonal antibody, GK1.5 or 2.43, respectively, administered one day (24 h) prior to infection was sufficient to limit the development of the paralytic syndrome by 79% (GK1.5) and 82% (2.43).

Documentos Relacionados

• Regulation of immunity by anti-T-cell antibodies.
• Physical association of CD4 and the T-cell receptor can be induced by anti-T-cell receptor antibodies.
• A Central Role for CD4+ T Cells and RANTES in Virus-Induced Central Nervous System Inflammation and Demyelination
• Differential Influence of Interleukin-12 in the Pathogenesis of Autoimmune and Virus-Induced Central Nervous System Demyelination
• Treatment of Guillain-Barré syndrome with anti-T cell monoclonal antibodies.