Bcl11b is required for differentiation and survival of αβ T lymphocytes

被引:292
作者
Wakabayashi, Y
Watanabe, H
Inoue, J
Takeda, N
Sakata, J
Mishima, Y
Hitomi, J
Yamamoto, T
Utsuyama, M
Niwa, O
Aizawa, S
Kominami, R
机构
[1] Niigata Univ, Grad Sch Med & Dent Sci, Dept Mol Genet, Niigata 9518122, Japan
[2] Univ Ryukyus, Ctr Mol Biosci, Div Cellular & Mol Immunol, Okinawa 9030213, Japan
[3] Kumamoto Univ, Inst Mol Embryol & Genet, Kumamoto 8600811, Japan
[4] Niigata Univ, Grad Sch Med & Dent Sci, Dept Cellular Funct, Niigata 9518122, Japan
[5] Tokyo Med & Dent Univ, Grad Sch, Dept Pathol & Immunol, Bunkyo Ku, Tokyo 1138519, Japan
[6] Kyoto Univ, Ctr Radiat Biol, Sakyo Ku, Kyoto 6068315, Japan
关键词
D O I
10.1038/ni927
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The gene Bcl11b, which encodes zinc finger proteins, and its paralog, Bcl11a, are associated with immune-system malignancies. We have generated Bcl11b-deficient mice that show a block at the CD4(-)CD8(-) double-negative stage of thymocyte development without any impairment in cells of B- or gammadelta T cell lineages. The Bcl11b(-/-) thymocytes showed unsuccessful recombination of V-beta to D-beta and lacked the pre-T cell receptor (TCR) complex on the cell surface, owing to the absence of Tcrb mRNA expression. In addition, we saw profound apoptosis in the thymus of neonatal Bcl11b(-/-) mice. These results suggest that Bcl11b is a key regulator of both differentiation and survival during thymocyte development.
引用
收藏
页码:533 / 539
页数:7
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