1. Targeting T cells responsive to the priming epitope prevent the relapsing phase of experimental autoimmune encephalomyelitis.
- Author
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Wegmann KW, Bouwer HG, Gregory CR, Whitham RH, and Hinrichs DJ
- Subjects
- Acute Disease, Animals, Cell Movement immunology, Claudins pharmacology, Female, Immunization, Immunologic Memory immunology, Mice, Mice, Inbred Strains, Peptide Fragments immunology, Secondary Prevention, T-Lymphocytes pathology, Claudins immunology, Encephalomyelitis, Autoimmune, Experimental immunology, Encephalomyelitis, Autoimmune, Experimental pathology, Encephalomyelitis, Autoimmune, Experimental prevention & control, Epitopes, T-Lymphocyte immunology, Immunotherapy methods, Peptide Fragments pharmacology, T-Lymphocytes immunology
- Abstract
Upon recovery from the initial episode of experimental autoimmune encephalomyelitis (EAE), virtually all SJL mice develop relapsing/remitting episodes of disease. These relapses may occur due to the reactivation of memory T cells initially stimulated as part of the disease-inducing protocol or naïve T-cell populations stimulated by distinct encephalitogens derived from the inflammatory disease process (epitope spread). We have used encephalitogen-specific non-linear peptide octamers to modify the course of relapsing EAE (rEAE) in SJL mice immunized with an oliogodendrocyte-specific protein peptide (OSP 55-71). Our studies show that the peptide-octamers, which target the T cells stimulated by the priming encephalitogen, but not other candidate encephalitogens, prevent rEAE., (Published by Elsevier B.V.)
- Published
- 2013
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