Investigative ophthalmology & visual science · 2004
Myelin/oligodendrocyte glycoprotein-specific T-cells induce severe optic neuritis in the C57BL/6 mouse.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод пока не подготовлен
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Shao Hui, Huang Zhigang, Sun Sheher L, Kaplan Henry J, Sun Deming
Аннотация
PURPOSE: The optic nerve is a common site of tissue damage in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). To determine the relationship between optic neuritis (ON) and EAE, we examined the incidence of ON in C57BL/6 (B6) mice immunized with a myelin oligodendrocyte/glycoprotein (MOG)-derived peptide or injected with MOG-specific T cells, which are known to induce EAE.
METHODS: Mice were immunized with MOG35-55 or MOG40-54 peptides emulsified in complete Freund's adjuvant (CFA). Pertussis toxin (PTX) was injected intraperitoneally 1 day before and after immunization. For disease induction by adoptive transfer of primed cells, donor C57BL/6 mice were received with T-cell blasts (1-6 x 10(6)/mouse). Both EAE and ON were observed by either clinical signs or histology.
RESULTS: ON developed in a high proportion of B6 mice treated with either protocol. The most severe inflammation was observed in the adoptively transferred mice. The induced ON was most frequently bilateral. In either actively or adoptively transferred diseases, both association and dissociation of EAE and ON was observed.
CONCLUSIONS: Different MOG-specific T-cell subsets might be involved in the pathogenesis of EAE and ON. A better understanding of the pathogenesis of ON after induction by MOG may have important diagnostic and therapeutic implications.
METHODS: Mice were immunized with MOG35-55 or MOG40-54 peptides emulsified in complete Freund's adjuvant (CFA). Pertussis toxin (PTX) was injected intraperitoneally 1 day before and after immunization. For disease induction by adoptive transfer of primed cells, donor C57BL/6 mice were received with T-cell blasts (1-6 x 10(6)/mouse). Both EAE and ON were observed by either clinical signs or histology.
RESULTS: ON developed in a high proportion of B6 mice treated with either protocol. The most severe inflammation was observed in the adoptively transferred mice. The induced ON was most frequently bilateral. In either actively or adoptively transferred diseases, both association and dissociation of EAE and ON was observed.
CONCLUSIONS: Different MOG-specific T-cell subsets might be involved in the pathogenesis of EAE and ON. A better understanding of the pathogenesis of ON after induction by MOG may have important diagnostic and therapeutic implications.