Key result
GMCSF-MOG or GMCSF-PLP fusion proteins block EAE development and progression in murine models.
Why the study?
Does a GM-CSF and myelin auto-antigen fusion protein prevent the development and progression of EAE in murine models?
Does a GM-CSF and myelin auto-antigen fusion protein prevent the development and progression of EAE in murine models?
Fusion proteins containing GM-CSF coupled to myelin auto-antigens elicit tolerance and block EAE progression in murine models, suggesting potential as therapeutic vaccines for multiple sclerosis.
Should not yet inform multiple sclerosis care; leaves open translation of GM-CSF fusion tolerance from murine EAE.
BACKGROUND: Vaccination strategies that elicit antigen-specific tolerance are needed as therapies for autoimmune disease. This study focused on whether cytokine-neuroantigen (NAg) fusion proteins could inhibit disease in chronic murine models of experimental autoimmune encephalomyelitis (EAE) and thus serve as potential therapeutic modalities for multiple sclerosis. RESULTS: A fusion protein comprised of murine GM-CSF as the N-terminal domain and the encephalitogenic MOG35-55 peptide as the C-terminal domain was tested as a tolerogenic, therapeutic vaccine (TTV) in the C57BL/6 model of EAE. Administration of GMCSF-MOG before active induction of EAE, or alternatively, at the onset of EAE blocked the development and progression of EAE. Covalent linkage of the GM-CSF and MOG35-55 domains was required for tolerogenic activity. Likewise, a TTV comprised of GM-CSF and PLP139-151 was a tolerogen in the SJL model of EAE. CONCLUSION: These data indicated that fusion proteins containing GM-CSF coupled to myelin auto-antigens elicit tolerance rather than immunity.
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Abbott et al. (2011) studied Experimental autoimmune encephalomyelitis (EAE). GMCSF-MOG and GMCSF-PLP fusion proteins vs. Saline, MOG35-55, PLP139-151, or GM-CSF alone was evaluated on Incidence and severity of EAE. Administration of GMCSF-MOG or GMCSF-PLP fusion proteins before or after the onset of experimental autoimmune encephalomyelitis blocked the development and progression of the disease in murine models.
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