The Constitutive Tyrosine Phosphorylation of CD3ζ Results from TCR-MHC Interactions That Are Independent of Thymic Selection1
The Constitutive Tyrosine Phosphorylation of CD3ζ Results from TCR-MHC Interactions That Are Independent of Thymic Selection1
复制标题
CD3z 的组成型酪氨酸磷酸化来自与胸腺选择无关的 TCR-MHC 相互作用1
作者：
Amy M Becker;Laura M. DeFord;C. Wuelfing;N. V. van Oers
从胸腺细胞和外周T细胞中分离出的T细胞受体（TCR）复合物，含有一种持续发生酪氨酸磷酸化的CD3ζ分子，称为p21。先前的研究表明，CD3ζ的持续磷酸化源于TCR与胸腺和外周组织中主要组织相容性复合体（MHC）分子的相互作用。为了确定选择环境对这种持续磷酸化有何影响，我们分析了几种不同的I类和II类限制性TCR转基因小鼠的CD3ζ，这些小鼠的胸腺细胞发育分别处于有选择或无选择的MHC环境中。在此，我们报告称，在无选择的肽 - MHC条件下发育的胸腺细胞中存在持续磷酸化的CD3ζ（p21）。这些发现有力地支持了这样一种模型，即TCR在 repertoire选择之前对MHC分子就具有内在亲和力。对TCR刺激前后TCR复合物的生化分析表明，持续磷酸化的CD3ζ亚基对TCR从头产生的信号并无贡献。这些发现对于正常和自身免疫情况下自身MHC识别过程中的T细胞功能可能具有重要意义。
The TCR complex, when isolated from thymocytes and peripheral T cells, contains a constitutively tyrosine-phosphorylated CD3ζ molecule termed p21. Previous investigations have shown that the constitutive phosphorylation of CD3ζ results from TCR interactions with MHC molecules occurring in both the thymus and the periphery. To determine what contribution the selection environment had on this constitutive phosphorylation, we analyzed CD3ζ from several distinct class I- and II-restricted TCR-transgenic mice where thymocyte development occurred in either a selecting or a nonselecting MHC environment. Herein, we report that constitutively phosphorylated CD3ζ (p21) was present in thymocytes that developed under nonselecting peptide-MHC conditions. These findings strongly support the model that the TCR has an inherent avidity for MHC molecules before repertoire selection. Biochemical analyses of the TCR complex before and after TCR stimulation suggested that the constitutively phosphorylated CD3ζ subunit did not contribute to de novo TCR signals. These findings may have important implications for T cell functions during self-MHC recognition under normal and autoimmune circumstances.
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影响因子：
32.4
作者：
VANOERS, NSC;KILLEEN, N;WEISS, A
通讯作者：
WEISS, A
影响因子：
32.4
作者：
Daniels, MA;Levine, L;Jameson, SC
通讯作者：
Jameson, SC
影响因子：
32.4
作者：
Carpino, N;Turner, S;Ihle, JN
通讯作者：
Ihle, JN
通过改变的肽配体诱导 T 细胞拮抗作用不需要差异化 CD3 zeta 磷酸化。
DOI：
--
发表时间：
1999
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Liu,H;Vignali,DA
通讯作者：
Vignali,DA