Selective depletion of myelin–reactive T cells with the anti–OX–40 antibody ameliorates autoimmune encephalomyelitis

Authors:
  • DBD.N. Bourdette
    D.N. Bourdette
  • TST.J. Sullivan
    T.J. Sullivan
  • MLM. Lemon
    M. Lemon
  • RMR. Maziarz
    R. Maziarz
  • MDM. Davey
    M. Davey
  • FPF. Palida
    F. Palida
  • WGW. Godfrey
    W. Godfrey
  • EEE. Engleman
    E. Engleman
  • RFR.J. Fulton
    R.J. Fulton
  • HOH. Offner
    H. Offner
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Abstract
The OX-40 protein was selectively upregulated on encephalitogenic myelin basic protein (MBP)-specific T cells at the site of inflammation during the onset of experimental autoimmune encephalomyelitis (EAE). An OX-40 immunotoxin was used to target and eliminate MBP-specific T cells within the central nervous system without affecting peripheral T cells. When injected in vivo, the OX-40 immunotoxin bound exclusively to myelin-reactive T cells isolated from the CNS, which resulted in amelioration of EAE. Expression of the human OX-40 antigen was also found in peripheral blood of patients with acute graft-versus-host disease and the synovia of patients with rheumatoid arthritis during active disease. The unique expression of the OX-40 molecule may provide a novel therapeutic strategy for eliminating autoreactive CD4+T cells that does not require prior knowledge of the pathogenic autoantigen.

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