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Adoptively transferred EAE in mice bearing the lpr mutation
R B Clark1, M Grunnet, E G Lingenheld
1Division of Rheumatic Diseases, University of Connecticut School of Medicine, Farmington 06032, USA.
Clinical Immunology and Immunopathology
|December 24, 1997
Summary
Mice lacking Fas/FasL are susceptible to experimental allergic encephalomyelitis (EAE), suggesting this cell death pathway is not integral to acute EAE effector phase. This research aids understanding of EAE pathogenesis.
Area of Science:
- Neuroimmunology
- Autoimmune Diseases
- T cell immunology
Background:
- Experimental Allergic Encephalomyelitis (EAE) is a mouse model for Multiple Sclerosis (MS).
- Fas/FasL-mediated apoptosis is implicated in MS pathogenesis.
- Generating encephalitogenic T cell clones from resistant mouse strains allows gene function analysis in EAE.
Purpose of the Study:
- To investigate the role of Fas/FasL-mediated cell death in the effector phase of EAE.
- To determine if Fas-deficient mice are susceptible to EAE induced by encephalitogenic T cell clones.
Main Methods:
- Generation of encephalitogenic T cell clones from wild-type C57BL/6 mice.
- Adoptive transfer of these T cell clones into Fas-deficient C57BL/6-lpr mice.
- Assessment of EAE induction and progression in recipient mice.
Main Results:
- Fas-deficient C57BL/6-lpr mice were fully susceptible to the adoptive transfer of EAE.
- The presence of functional Fas/FasL signaling was not required for EAE induction in this model.
- These findings challenge the proposed role of Fas/FasL in the acute effector phase of EAE.
Conclusions:
- Fas/FasL-mediated cell death in the central nervous system does not play an integral role in the effector phase of acute EAE.
- Further research is needed to elucidate the precise mechanisms of T cell-mediated pathology in EAE and MS.