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Brain, Vol. 116, No. 5, 1043-1058, 1993
© 1993 Guarantors of Brain

research-article

Suppression of experimental allergic neuritis by an antibody to the intercellular adhesion molecule ICAM-1

Juan J. Archelos, Mathias Mäurer, Stefan Jung, Klaus V. Toyka and Hans-Peter Hartung

Department of Neurology, Neuroimmunology Branch and Clinical Research Group for Multiple Sclerosis, Julius-Maximillions-Universität Würzburg Würzburg, Germany

Correspondence to: Correspondence to J J Archelos, Neurologische Klinik der Universität Würzburg, Josef-Schneider Str. 11, W-97080 Würzburg, Germany.

Experimental allergic (autoimmune) neuritis (EAN) was induced in Lewis rats either by inoculation with bovine spinal root myelin or injection of neuritogenic P2-specific T cells. Injection of a purified monoclonal antibody (1A–29) to the intercellular adhesion molecule-1 (ICAM-1) prevented or transiently suppressed myelin-induced EAN depending on the timing of antibody application. Administration of 1A-29 suppressed moderate adoptive transfer EAN (AT-EAN) but not severe AT-EAN. In contrast, treatment with phosphate buffered saline or an unrelated IgG1 had no effect on the course of the disease. Histological sections of the peripheral nervous system (PNS) showed a marked reduction of inflammatory infiltrates and perivascular demyelination in rats injected with 1A-29. The effect of 1A-29 on the concanavalin A (Con A)- and P2-dependent proliferation of neuritogenic P2-specific T cells was studied in vitro. Our data suggest that antibodies to ICAM-1 act on the induction and effector phase of the immune response by inhibiting both early interactions between immunocompetent cells after exposure to foreign antigen and transendothelial migration of primed T cells into the peripheral nerve.

Treatment with antibodies to leucocyte adhesion molecules could be a useful therapeutic approach to autoimmune disease of the PNS.

Received December 2, 1992. Revised February 10, 1993. Accepted May 26, 1993.


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