Induction of experimental autoimmune neuritis in CD4 −8 − C57BL/6J mice

Abstract

The C57BL/6J mice strain is known to be reputedly resistant to induction of experimental autoimmune neuritis (EAN), an animal model of Guillain–Barré syndrome in humans. Here we describe the induction of EAN in mice of the C57BL/6J background by transfer into naive syngeneic recipients bovine peripheral nerve myelin (BPM)-primed donor lymph node cells that had been stimulated in vitro with the bovine peripheral nervous system (PNS) myelin P2 protein peptide 57–81 followed by challenge with BPM, Freund's complete adjuvant and pertussis toxin. EAN was more severe, both clinically and histologically, and accompanied by extensive infiltration of inflammatory cells and demyelination in peripheral nerves when examined on day 30 after transfer of primed T cells from CD4 −8 − mice into identical naive hosts than after transfer of cells from primed wild type, CD4 −/ − or CD8 −/ − mice to corresponding recipient animals. EAN in CD4 −8 − mice was also associated with elevated numbers of P2 peptide-reactive interferon-γ (IFN-γ) secreting cells and αβ T cells were present in lymph nodes and spleens. The data suggest that PNS myelin activated T cells from an EAN-resistant mice strain are capable of homing to the PNS. The expanded CD4 −8 − αβ T cells may have helper and effector functions, related to initiation of EAN in the CD4 −8 − mice. Lack of CD4 + and CD8 + expressing cells does not prevent the initiation of an autoimmune disease.