Abstract
Abstract Deep cervical lymph nodes (dcLNs) were reported to be the first location for the initiation of encephalitogenic CD4+ T cells in experimental autoimmune encephalomyelitis (EAE). However, the precise mechanisms are not crystal clear. Here, we explored the epitope spreading in the two anatomically adjacent diseases, periodontitis and EAE. C57bl/6 mice were immunized with porphyromonas gingivalis (p.gingivalis), a virulent peridontopathogen, in the buccal submucosal tissue. Activation of T cells and MOG-specific CD4+ T cells in dcLNs and superficial cervical lymph nodes were detected with respect to the expression of CD69, CD44, and MOG-tetramer. A clinical symptom was observed in p.gingivalis-immunzed mice similar to that in MOG35-55 peptide-immunized mice. Dendritic cells in the buccal submucosal tissue and dcLNs were analyzed for the spreading of MOG epitope. Our results demonstrated the existence of the epitope spreading to the endogenous myelin in the inflammatory reponse of periodontitis caused by infection of p.gingivalis.
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