the degradation of lipids. Consequently, CD83 might not only mark activated cells but also be indicative of cells important for the clearance of debris and initiating the resolution of inflammation. Similarly, we have described that CD83-deficiency in DCs and macrophages subverts their capacity to regulate immune responses, eventually resulting in aggravated autoimmunity and hampered resolution of inflammation16,18. In this respect, it is worth mentioning that CX3CR1-CreERT2-driven depletion of Cd83 can affect border-associated macrophages, which were also shown to express Cd8320. Although we have demonstrated that disease severity in CD83ΔMG mice clearly correlates with an exaggerated activation status of CD83-deficient microglia, we cannot fully exclude a contribution of targeted border-associated macrophages to the observed phenotype.
