Ardouin L, Ismaili J, Malissen B, Malissen M
Centre d'Immunologie Institut National de la Santé et de la Recherche Médicale-Centre National de la Recherche Scientifique de Marseille-Luminy, Case 906, 13288 Marseille Cedex 9, France.
J Exp Med. 1998 Jan 5;187(1):105-16. doi: 10.1084/jem.187.1.105.
The pre-T cell receptor (TCR) associates with CD3-transducing subunits and triggers the selective expansion and maturation of T cell precursors expressing a TCR-beta chain. Recent experiments in pre-Talpha chain-deficient mice have suggested that the pre-TCR may not be required for signaling allelic exclusion at the TCR-beta locus. Using CD3-epsilon- and CD3-zeta/eta-deficient mice harboring a productively rearranged TCR-beta transgene, we showed that the CD3-gammadeltaepsilon and CD3-zeta/eta modules, and by inference the pre-TCR/CD3 complex, are each essential for the establishment of allelic exclusion at the endogenous TCR-beta locus. Furthermore, using mutant mice lacking both the CD3-epsilon and CD3-zeta/eta genes, we established that the CD3 gene products are dispensable for the onset of V to (D)J recombination (V, variable; D, diversity; J, joining) at the TCR-beta, TCR-gamma, and TCR-delta loci. Thus, the CD3 components are differentially involved in the sequential events that make the TCR-beta locus first accessible to, and later insulated from, the action of the V(D)J recombinase.
前T细胞受体（TCR）与CD3转导亚基结合，并触发表达TCR-β链的T细胞前体的选择性扩增和成熟。最近在前Tα链缺陷小鼠中的实验表明，TCR-β基因座的信号等位基因排斥可能不需要前TCR。利用携带有效重排的TCR-β转基因的CD3-ε和CD3-ζ/η缺陷小鼠，我们发现CD3-γδε和CD3-ζ/η模块，以及由此推断的前TCR/CD3复合物，对内源性TCR-β基因座等位基因排斥的建立都是必不可少的。此外，利用同时缺乏CD3-ε和CD3-ζ/η基因的突变小鼠，我们确定CD3基因产物对于TCR-β、TCR-γ和TCR-δ基因座的V到（D）J重组（V，可变区；D，多样区；J，连接区）的起始是可有可无的。因此，CD3组分以不同方式参与了一系列事件，这些事件使得TCR-β基因座首先能够被V（D）J重组酶作用，随后又能免受其作用。
