淋巴毒素β受体控制外周淋巴组织中的器官发生和亲和力成熟。

The lymphotoxin beta receptor controls organogenesis and affinity maturation in peripheral lymphoid tissues.

作者信息

Fütterer A, Mink K, Luz A, Kosco-Vilbois M H, Pfeffer K

机构信息

Institute of Medical Microbiology, Immunology, and Hygiene, Technical University of Munich, Germany.

出版信息

Immunity. 1998 Jul;9(1):59-70. doi: 10.1016/s1074-7613(00)80588-9.

DOI:10.1016/s1074-7613(00)80588-9

PMID:9697836

Abstract

Lymphotoxin beta receptor (LTbetaR)-/- mice were created by gene targeting. LTbetaR-/- mice lacked Peyer's patches, colon-associated lymphoid tissues, and all lymph nodes. Mucosa patrolling alphaEbeta7high integrin+ T cells were virtually absent. Spleens lost marginal zones; T/B cell segregation and follicular dendritic cell networks were absent. Peanut agglutinin+ cells were aberrantly detectable around central arterioles. In contrast to TNF receptor p55-/- mice, antibody affinity maturation was impaired. Since LTbetaR-/- mice exhibit distinct defects when compared to LTalpha-/- and LTbeta-/- mice, it is suggested that the LTbetaR integrates signals from other TNF family members. Thus, the LTbetaR proves pivotal for the ontogeny of the secondary lymphoid tissues. Furthermore, affinity maturation is dependent on LTalpha1beta2 rather than on LTalpha3.

摘要

通过基因靶向技术构建了淋巴毒素β受体（LTbetaR）基因敲除小鼠。LTbetaR基因敲除小鼠缺乏派尔集合淋巴结、结肠相关淋巴组织和所有淋巴结。几乎不存在黏膜巡逻的αEβ7高整合素+ T细胞。脾脏失去边缘区；T/B细胞分离和滤泡树突状细胞网络缺失。在中央小动脉周围可异常检测到花生凝集素+细胞。与TNF受体p55基因敲除小鼠相比，抗体亲和力成熟受损。由于与LTalpha基因敲除和LTbeta基因敲除小鼠相比，LTbetaR基因敲除小鼠表现出不同的缺陷，提示LTbetaR整合来自其他TNF家族成员的信号。因此，LTbetaR被证明对次级淋巴组织的个体发育至关重要。此外，亲和力成熟依赖于LTalpha1beta2而非LTalpha3。