Negative regulation of activation-induced cytidine deaminase in B cells

被引：72

作者：

Muto, T

Okazaki, IM

Yamada, S

Tanaka, Y

Kinoshita, K

Muramatsu, M

Nagaoka, H

Honjo, T ^{[1
]}

机构：

[1] Kyoto Univ, Dept Immunol & Genom Med, Grad Sch Med, Sakyo Ku, Kyoto 6068501, Japan

[2] Kyoto Univ, PRESTO, Japan Sci & Technol Corp, Sakyo Ku, Kyoto 6068501, Japan

[3] Kyoto Univ, Lab Immunol & Cell Biol, Grad Sch Biostudies, Sakyo Ku, Kyoto 6068501, Japan

[4] Akita Univ, Anim Res Lab, Biosci Res & Educ Ctr, Akita 0108543, Japan

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2006年 / 103卷 / 08期

关键词：

antibodies; protein modification; transgenic/knockout mice;

D O I：

10.1073/pnas.0510970103

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Both class switch recombination (CSR) and somatic hypermutation (SHIM) of the Ig genes require the activity of activation-induced cytidine deaminase (AID). Expression of AID is restricted to B cells in the germinal centers of the lymphoid organs, where activated B cells undergo CSR and SHM. We previously showed that constitutive and systemic expression of AID leads to tumorigenesis in T cells and lung epithelium, but not in B cells. This finding led us to suspect that transgenic AID may be inactivated at least in part in B cells. To address this issue, we generated conditional AID-transgenic mice that constitutively express AID only in B cells. Studies on the cross between the AID-transgenic and AID-deficient mice showed that abundant AID protein accumulated by constitutive expression is inactivated in B cells, possibly providing an explanation for the absence of deregulation of CSR and SHM in AID-transgenic B cells.

引用

页码：2752 / 2757

页数：6