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Anti-T-cell receptor V beta 6 breaks tolerance in Mlsa mice and induces production of anti-Mlsa antibodies.

机译:抗T细胞受体V beta 6破坏了Mlsa小鼠的耐受性并诱导了抗Mlsa抗体的产生。

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摘要

Tolerance to the minor lymphocyte stimulating (Mls) self-antigens has been shown to be due to the intrathymic deletion of T-cell clones bearing certain T-cell receptor (TcR) V beta regions. T cells bearing these V beta regions (V beta 6, V beta 7, V beta 8.1, V beta 9) are deleted in Mlsa-positive mice. This report demonstrates that hyperimmunization of AKR mice with anti-V beta 6 breaks tolerance to the self-antigen Mlsa and induces the development of anti-Mlsa antibodies. These antibodies had the capacity to block Mlsa-induced mixed lymphocyte responses between H-2 identical strain combinations and also between Mlsa-congeneic BALB.D2MA and parental BALB/c strains. Furthermore, when the responder lymphocytes were Mlsa-positive their response to allogeneic major or minor histocompatibility antigens was enhanced in the presence of this antiserum. This indicates that Mlsa may be present on T cells and that occupancy of this ligand leads to enhanced signal transduction.
机译:已显示出对次要淋巴细胞刺激(Mls)自体抗原的耐受性是由于胸腺内删除带有某些T细胞受体(TcR)Vβ区域的T细胞克隆。在Msa阳性小鼠中删除了带有这些V beta区域(V beta 6,V beta 7,V beta 8.1,V beta 9)的T细胞。该报告证明,用抗Vβ6的AKR小鼠进行超免疫会破坏对自身抗原Mlsa的耐受性,并诱导抗Mlsa抗体的产生。这些抗体具有阻断H-2相同菌株组合之间以及Msa同源BALB.D2MA和亲代BALB / c菌株之间Msa诱导的混合淋巴细胞反应的能力。此外,当反应者淋巴细胞Mlsa阳性时,在这种抗血清的存在下,它们对同种异体主要或次要组织相容性抗原的反应增强。这表明M1sa可能存在于T细胞上,并且该配体的占据导致增强的信号转导。

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