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International Immunology, Vol. 11, No. 12, 1889-1896, December 1999
© 1999 Japanese Society for Immunology

The role of CTLA-4 in tolerance induction and Ttigen administration cell differentiation in experimental autoimmune encephalomyelitis: i.v. 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

Interactions between B7 molecules on antigen-presenting cells and CTLA-4 on T cells have been shown to be important in establishing tolerance. In the present study, we examined the kinetics of tolerance induction following i.v. 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 (LNC) response 10 days after antigen administration demonstrated an accentuation of i.v. tolerance induction with anti-CTLA-4 blockade. Anergy was induced in splenocytes by i.v. antigen administration as shown by a decrease in MBP-specific proliferation and IL-2 production, and anti-CTLA-4 potentiated this effect. In addition, i.v. antigen plus anti-CTLA-4 and complete Freund's adjuvant was not encephalitogenic. Interestingly, i.v. tolerance (a single injection) did not inhibit experimental autoimmune encephalomyelitis (EAE) and anti-CTLA-4 administration did not alter this phenotype. These results suggest that while the majority of MBP-specific T cells are tolerized by i.v. antigen and that this process is potentiated by anti-CTLA-4 administration, a population of T cells remains that is quite efficient in mediating EAE.

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

Transmitting editor: L. Steinman


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R. B. Ratts, L. R. Arredondo, P. Bittner, P. J. Perrin, A. E. Lovett-Racke, and M. K. Racke
The role of CTLA-4 in tolerance induction and T cell differentiation in experimental autoimmune encephalomyelitis: i.p. antigen administration
Int. Immunol., December 1, 1999; 11(12): 1881 - 1888.
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