Abstract
A common theme found in studies with mouse models of autoimmune diseases is that pathogenic T cells are primarily responsible for the pathology. Such models include diabetes in non-obese diabetic (NOD) mice, experimental autoimmune encephalomyelitis (EAE)—a model of multiple sclerosis (MS), collagen II (CII)-induced arthritis (CIA)—a model of rheumatoid arthritis (RA). Pathogenic T cells in EAE utilize a restricted repertoire of genes encoding the T-cell receptor (TCR) (1). For example, upon immunization of H-2u mice with either myelin basic protein, or its immunodominant fragment, peptide Ac1-20, the Vβ8.2 TCR gene product is expressed in the majority of pathogenic T cells (2–4). The restricted usage of the Vβ8.2 TCR gene product has also been found in rats in which EAE was induced by a peptide of myelin basic protein (5). Similarly, a restriction in the TCR usage was found also in CII-induced arthritis in mice (6,7), and in the TCR alpha chain usage in non-obese diabetic (NOD) mice (8).
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Waisman, A. (2000). Immunity to T-Cell Receptor. In: Lowrie, D.B., Whalen, R.G. (eds) DNA Vaccines. Methods in Molecular Medicine™, vol 29. Humana Press. https://doi.org/10.1385/1-59259-688-6:397
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DOI: https://doi.org/10.1385/1-59259-688-6:397
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