Modulation of experimental autoimmune encephalomyelitis by administration of cells expressing antigenic peptide covalently linked to MHC class II

Abstract

The MHC class II molecule RT1B l covalently linked with gpMBP-71–90 was expressed in P80 cells (mouse mastocytoma P815 expressing rat-CD80) and i.v. injection ameleriorated active and adoptive transfer (AT) experimental autoimmune encephalomyelitis (EAE) in Lewis rats. Spinal cord of animals with AT-EAE showed significant increase of apoptotic T-cells at maximum of disease after injection of P80-RT1B l-MBP-71–90 but not of P80RT1B l or P80 cells. The data demonstrate a possible therapeutic effect on EAE by provision of T-cell receptor (TCR) and costimulatory signals by genetically engineered antigen presenting cells (APC) and suggest induction of T-cell apoptosis as important mechanism of action.