Asymmetric B Cell Division in the Germinal Center Reaction

被引:73
|
作者
Barnett, Burton E. [1 ,3 ]
Ciocca, Maria L. [1 ,3 ]
Goenka, Radhika [2 ]
Barnett, Lisa G. [3 ]
Wu, Junmin [1 ,3 ]
Laufer, Terri M. [3 ,4 ]
Burkhardt, Janis K. [2 ,5 ]
Cancro, Michael P. [2 ]
Reiner, Steven L. [1 ,3 ]
机构
[1] Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA
[2] Univ Penn, Perelman Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA
[3] Univ Penn, Perelman Sch Med, Dept Med, Philadelphia, PA 19104 USA
[4] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA 19104 USA
[5] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA
关键词
T-LYMPHOCYTE DIVISION; BCL-6; ANTIGEN; DIFFERENTIATION; INFLAMMATION; EXPRESSION; RESPONSES;
D O I
10.1126/science.1213495
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
Lifelong antibody responses to vaccination require reorganization of lymphoid tissue and dynamic intercellular communication called the germinal center reaction. B lymphocytes undergo cellular polarization during antigen stimulation, acquisition, and presentation, which are critical steps for initiating humoral immunity. Here, we show that germinal center B lymphocytes asymmetrically segregate the transcriptional regulator Bcl6, the receptor for interleukin-21, and the ancestral polarity protein atypical protein kinase C to one side of the plane of division, generating unequal inheritance of fate-altering molecules by daughter cells. Germinal center B lymphocytes from mice with a defect in leukocyte adhesion fail to divide asymmetrically. These results suggest that motile cells lacking constitutive attachment can receive provisional polarity cues from the microenvironment to generate daughter cell diversity and self-renewal.
引用
收藏
页码:342 / 344
页数:3
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