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This strategy requires no external adjuvant, likely because the recombinant hepatitis B core antigen (HBcAg) carries nucleic acids that act as TLR-3 agonists [118]
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To account for the continuing degeneration and atrophy in later stages, in the face of waning adaptive inflammation as the disease progresses, it has been proposed that the inflammation becomes “trapped” behind the blood–brain barrier, continuing to damage the CNS, but now being inaccessible to peripherally-administered immunosuppressants
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