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International Immunology, Vol. 11, No. 12, 1881-1888, December 1999
© 1999 Japanese Society for Immunology

The role of CTLA-4 in tolerance induction and T cell differentiation in experimental autoimmune encephalomyelitis: i.p. antigen administration

Robert B. Ratts, Lachelle R. Arredondo, Patrice Bittner, Peter J. Perrin1, Amy E. Lovett-Racke and Michael K. Racke

Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
1 Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA

Correspondence to: M. K. Racke, Department of Neurology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9036, USA

Recent evidence suggests that co-stimulation provided by B7 molecules through CTLA-4 is important in establishing peripheral tolerance. In the present study, we examined the kinetics of tolerance induction and T cell differentiation following i.p. administration of myelin basic protein (MBP) Ac1–11 in mice transgenic for a TCR Vß8.2 gene derived from an encephalitogenic T cell clone specific for MBP Ac1–11. Examination of the lymph node cell response after antigen administration demonstrated a dependence on CTLA-4 for i.p. tolerance induction. Examination of splenocyte responses suggested that i.p. antigen administration induced a Th2 response, which was potentiated by anti-CTLA-4 administration. Interestingly, i.p. tolerance was able to inhibit the induction of experimental autoimmune encephalomyelitis and anti-CTLA-4 administration did not alter this phenotype, suggesting that CTLA-4 blockade did not block tolerance induction. Thus, T cell differentiation and the dependence on CTLA-4 for tolerance induction following i.p. antigen administration differs between lymph node and spleen in a model of organ-specific autoimmunity.

Keywords: experimental autoimmune encephalomyelitis, co-stimulatory molecules, neuroimmunology, tolerance


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