2000
DOI: 10.1002/1521-4141(2000)30:18<2164::aid-immu2164>3.3.co;2-n
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Induction of experimental autoimmune arthritis by a public epitope of the T cell receptor variable α  domain of an arthritogenic T cell clone

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Cited by 2 publications
(2 citation statements)
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“…The peptide 66-80 elicits classic delayed-type hypersensitivity, even in naive rats, suggesting that there is a preexisting level of T cell priming, and that this reactivity is increased in rats with AIA. In contrast, nasal application of the antiidiotypic V␣ peptide 66-80 results in a decrease both of subsequent arthritis and the accompanying delayed-type hypersensitivity (50).…”
Section: Regulation Driven By Idiotopes Of Effector T Cell Receptor Osupporting
confidence: 84%
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“…The peptide 66-80 elicits classic delayed-type hypersensitivity, even in naive rats, suggesting that there is a preexisting level of T cell priming, and that this reactivity is increased in rats with AIA. In contrast, nasal application of the antiidiotypic V␣ peptide 66-80 results in a decrease both of subsequent arthritis and the accompanying delayed-type hypersensitivity (50).…”
Section: Regulation Driven By Idiotopes Of Effector T Cell Receptor Osupporting
confidence: 84%
“…Recipients of a transfer of antiidiotype-specific cells become resistant to arthritis induced by M tuberculosis. In contrast to the V␤18 results, immunization of normal animals with V␣11 peptide 66-80 or antiidiotypic cells recognizing V␣11 peptide 66-80 leads to an arthritis (44,50). The peptide 66-80 elicits classic delayed-type hypersensitivity, even in naive rats, suggesting that there is a preexisting level of T cell priming, and that this reactivity is increased in rats with AIA.…”
Section: Regulation Driven By Idiotopes Of Effector T Cell Receptor Omentioning
confidence: 89%