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

来源：

NATURE IMMUNOLOGY | 2003年 / 4卷 / 06期

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

页码：533 / 539

页数：7

共 46 条

[41] Pleiotropic changes controlled by the pre-T-cell receptor [J].