Abstract
BackgroundImmunity against the T cell receptor (TCR) is considered to play a central role in the regulation of experimental allergic encephalomyelitis (EAE), a model system of autoimmune disease characterized by a restricted usage of TCR genes. Methods of specific vaccination against the TCR of pathogenetic T cells have included attenuated T cells and synthetic peptides from the sequence of the TCR. These approaches have led to the concept that anti-idiotypic immunity against antigenic sites of the TCR, which are a key regulatory element in this disease.MethodsThe present study in the Lewis rat used a conventional idiotypic immunization based on antigenized antibodies expressing selected peptide sequences of the Vβ8.2 TCR (93ASSDSSNTE101 and 39DMGHGLRLIHYSYDVNSTEKG59).ResultsThe study demonstrates that vaccination with antigenized antibodies markedly attenuates, and in some instances, prevents clinical EAE induced with the encephalitogenic peptide 68GSLPQKSQRSQDENPVVHF88 in complete Freunds' adjuvant (CFA). Antigenized antibodies induced an anti-idiotypic response against the Vβ8.2 TCR, which was detected by ELISA and flowcytometry. No evidence was obtained of a T cell response against the corresponding Vβ8.2 TCR peptides.ConclusionsThe results indicate that antigenized antibodies expressing conformationally-constrained TCR peptides are a simple means to induce humoral anti-idiotypic immunity against the TCR and to vaccinate against EAE. The study also suggests the possibility to target idiotypic determinants of TCR borne on pathogenetic T cells to vaccinate against disease.
Highlights
Experimental allergic encephalomyelitis (EAE) is an experimentally induced autoimmune disease mediated by T cells
The results show that vaccination with antigenized antibodies expressing sequences of encephalitogenic T cells induces anti-idiotypic immunity against the T cell receptor (TCR) and high level resistance against EAE
Rats were vaccinated with an individual antigenized antibody and received a booster injection 21 days later
Summary
Experimental allergic encephalomyelitis (EAE) is an experimentally induced autoimmune disease mediated by T cells It can be induced in susceptible animals either by immunization with myelin basic protein (MBP) or proteolipid protein PLP, or by immunization with synthetic peptides from the MBP sequence [1]. Owing to similarities in clinical expression and histopathology, EAE has long been recognized as an animal model for multiple sclerosis, a demyelinating chronic inflammatory disease in humans of unknown origin. For this reason, studies on EAE are thought to elucidate aspects of the pathogenesis and indicate possible ways of immune intervention. These approaches have led to the concept that anti-idiotypic immunity against antigenic sites of the TCR, which are a key regulatory element in this disease
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