In summary, we have provided experimental evidence that microglial CD83 expression modulates the reaction to neuro-inflammatory damage in the CNS. CD83-deficient microglia mount an excessive pro-inflammatory response, marked by elevated production of chemokines, which recruit pathogenic cells to the site of inflammation. Together, these cells create a toxic environment fostering tissue damage and thus perpetuating paralytic symptoms. These data disclose that CD83 expression by microglia is not simply a marker molecule but rather a gatekeeper of cellular activation during neuroinflammation.
