Pullen A M, Marrack P, Kappler J W
Howard Hughes Medical Institute, National Jewish Center, Denver, CO.
J Immunol. 1989 May 1;142(9):3033-7.
V beta 3+ T cells are eliminated in Mls-2a mice carrying some, but not all, H-2 types. Analysis of AKXD and BXD recombinant inbred strains showed that Mls-2a (formerly Mlsc) was not the product of a single gene and suggested that at least two non-H-2 genes control V beta 3 levels. Studies of the progeny of a B10.BR x (C3H/HeJ x B10.BR)F1 backcross confirmed the existence of two V beta 3+ T cell deleting genes: one unlinked and one linked to Ly-7, which we propose be called Mls-2 and Mls-3, respectively. Mls-2a induces partial deletion of V beta 3+ T cells with a bias toward deleting CD4+ cells. It stimulates V beta 3+ hybrids and may be linked to Mtv-13 on chromosome 4. A third non-H-2 gene is implicated in enhancing the presentation of Mls-2a. Mls-3a causes elimination of all V beta 3+ T cells in H-2k and H-2d mice but poorly stimulates V beta 3+ hybrids.
在携带部分而非全部H-2类型的Mls-2a小鼠中，Vβ3⁺ T细胞会被清除。对AKXD和BXD重组近交系的分析表明，Mls-2a（以前称为Mlsc）不是单个基因的产物，并提示至少有两个非H-2基因控制Vβ3水平。对B10.BR x (C3H/HeJ x B10.BR)F1回交后代的研究证实了存在两个Vβ3⁺ T细胞缺失基因：一个不连锁，一个与Ly-7连锁，我们建议分别将它们称为Mls-2和Mls-3。Mls-2a诱导Vβ3⁺ T细胞部分缺失，且偏向于删除CD4⁺细胞。它刺激Vβ3⁺杂交细胞，可能与4号染色体上的Mtv-13连锁。第三个非H-2基因与增强Mls-2a的呈递有关。Mls-3a导致H-2k和H-2d小鼠中所有Vβ3⁺ T细胞被清除，但对Vβ3⁺杂交细胞的刺激较弱。
