Infection of mice with lactic dehydrogenase virus prevents development of experimental allergic encephalomyelitis
Journal of Neuroimmunology
|March 1, 1986
Abstract:
A significant reduction in the incidence of experimental allergic encephalomyelitis (EAE) in SJL/J mice was observed when mice were infected with lactic dehydrogenase virus (LDV) 14 days before, on day 0, or 3 days after immunization with spinal cord homogenate. These results are discussed in terms of the selective infection by LDV of I-region-associated antigen- (Ia) positive macrophages.
Insights
Lactic dehydrogenase virus (LDV) infection significantly reduced experimental allergic encephalomyelitis (EAE) in mice. This protective effect is linked to LDV
Area of Science:
- Immunology
- Virology
- Neuroscience
Background:
- Experimental allergic encephalomyelitis (EAE) is an autoimmune disease model for multiple sclerosis.
- Macrophages play a crucial role in the pathogenesis of EAE.
Purpose of the Study:
- To investigate the effect of lactic dehydrogenase virus (LDV) infection on the development of EAE.
- To explore the underlying mechanisms of LDV-mediated protection against EAE.
Main Methods:
- Induction of EAE in SJL/J mice using spinal cord homogenate.
- Infection of mice with LDV at different time points relative to immunization.
- Assessment of EAE incidence and severity.
- Analysis of macrophage populations and their antigen presentation capabilities.
Main Results:
- LDV infection administered 14 days before, on day 0, or 3 days after immunization significantly reduced EAE incidence.
- The protective effect of LDV was associated with the selective infection of I-region-associated antigen- (Ia) positive macrophages.
Conclusions:
- LDV infection confers protection against EAE in a mouse model.
- The mechanism involves the selective targeting of Ia-positive macrophages by LDV, potentially modulating the immune response.
