In this study, we delineate the specific roles of C5a receptor signaling and MAC formation during the progression of experimental autoimmune encephalomyelitis (EAE)-mediated neuroinflammation.
For example, mice lacking C5 and mice lacking the C5a receptor both develop experimental autoimmune encephalomyelitis (EAE) with the same frequency and intensity as their wild type counterparts.
Finally, using a combination of in situ hybridization and immunohistochemistry, we showed that the T cells infiltrating the central nervous system during experimental allergic encephalomyelitis express the C5aR mRNA.