4-1BB（CD137）配体/I-Eα转基因小鼠外周B淋巴细胞的进行性耗竭。

Progressive depletion of peripheral B lymphocytes in 4-1BB (CD137) ligand/I-Ealpha)-transgenic mice.

作者信息

Zhu G, Flies D B, Tamada K, Sun Y, Rodriguez M, Fu Y X, Chen L

机构信息

Department of Immunology, Mayo Graduate and Medical Schools, Mayo Clinic, Rochester, MN 55905, USA.

出版信息

J Immunol. 2001 Sep 1;167(5):2671-6. doi: 10.4049/jimmunol.167.5.2671.

DOI:10.4049/jimmunol.167.5.2671

PMID:11509610

Abstract

Interaction of 4-1BB (CD137) and its ligand (4-1BBL) is thought to positively regulate cell-mediated and humoral immune responses. We have prepared transgenic mouse strains that express 4-1BBL cDNA under the control of MHC class II I-Ealpha promoter. The 4-1BBL-transgenic mice show progressive splenomegaly and selective depletion of B220(+) B cells accompanied with low levels of circulating IgG and defective humoral responses to Ag challenge. In addition, splenocytes from the transgenic mice fail to provide stimulation for allogeneic T cells in both lymphoproliferative and CTL responses in vitro, whereas their T cells remain functionally normal. Our results reveal unexpected functions of 4-1BBL in the regulation of humoral immune responses and Ag presentation.

摘要

4-1BB（CD137）与其配体（4-1BBL）的相互作用被认为可正向调节细胞介导的和体液免疫反应。我们制备了在MHC II类I-Eα启动子控制下表达4-1BBL cDNA的转基因小鼠品系。4-1BBL转基因小鼠表现出进行性脾肿大以及B220(+) B细胞的选择性耗竭，同时伴有循环IgG水平降低以及对抗原刺激的体液反应缺陷。此外，转基因小鼠的脾细胞在体外淋巴细胞增殖和CTL反应中均无法为同种异体T细胞提供刺激，而它们的T细胞功能仍保持正常。我们的结果揭示了4-1BBL在体液免疫反应调节和抗原呈递中的意外功能。