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本文引用的文献

1
Engagement of the PD-1 immunoinhibitory receptor by a novel B7 family member leads to negative regulation of lymphocyte activation.一种新型B7家族成员与PD-1免疫抑制受体的结合导致淋巴细胞活化的负调节。
J Exp Med. 2000 Oct 2;192(7):1027-34. doi: 10.1084/jem.192.7.1027.
2
LICOS, a primordial costimulatory ligand?LICOS，一种原始共刺激配体？
Curr Biol. 2000 Mar 23;10(6):333-6. doi: 10.1016/s0960-9822(00)00383-3.
3
T cells: A proliferation of costimulatory molecules.T细胞：共刺激分子的增殖。
Curr Biol. 2000 Mar 23;10(6):R227-30. doi: 10.1016/s0960-9822(00)00400-0.
4
T-cell stimulation: an abundance of B7s.T细胞刺激：大量的B7分子。
Nat Med. 1999 Dec;5(12):1345-6. doi: 10.1038/70905.
5
Expression of B7 molecules in recipient, not donor, mice determines the survival of cardiac allografts.心脏异体移植的存活取决于受体小鼠而非供体小鼠中B7分子的表达。
J Immunol. 1999 Oct 1;163(7):3753-7.
6
The role of CTLA-4 in regulating Th2 differentiation.细胞毒性T淋巴细胞相关抗原4（CTLA-4）在调节辅助性T细胞2（Th2）分化中的作用。
J Immunol. 1999 Sep 1;163(5):2634-9.
7
CTLA-4 and T cell activation.细胞毒性T淋巴细胞相关抗原4与T细胞活化
Curr Opin Immunol. 1999 Jun;11(3):294-300. doi: 10.1016/s0952-7915(99)80047-8.
8
The role of CD80, CD86, and CTLA4 in alloimmune responses and the induction of long-term allograft survival.CD80、CD86和CTLA4在同种免疫反应及诱导长期同种异体移植存活中的作用。
J Immunol. 1999 Feb 15;162(4):1947-51.
9
ICOS is an inducible T-cell co-stimulator structurally and functionally related to CD28.诱导性共刺激分子（ICOS）是一种在结构和功能上与CD28相关的可诱导性T细胞共刺激分子。
Nature. 1999 Jan 21;397(6716):263-6. doi: 10.1038/16717.
10
B7-1 or B7-2 is required to produce the lymphoproliferative phenotype in mice lacking cytotoxic T lymphocyte-associated antigen 4 (CTLA-4).在缺乏细胞毒性T淋巴细胞相关抗原4（CTLA-4）的小鼠中，产生淋巴细胞增殖表型需要B7-1或B7-2。
J Exp Med. 1999 Jan 18;189(2):435-40. doi: 10.1084/jem.189.2.435.

缺乏CD28和CTLA4的小鼠中依赖B7的T细胞共刺激

B7-dependent T-cell costimulation in mice lacking CD28 and CTLA4.

作者信息

Mandelbrot D A, Oosterwegel M A, Shimizu K, Yamada A, Freeman G J, Mitchell R N, Sayegh M H, Sharpe A H

机构信息

Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.

出版信息

J Clin Invest. 2001 Apr;107(7):881-7. doi: 10.1172/JCI11710.

DOI:10.1172/JCI11710
PMID:11285307
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC199576/
Abstract

To examine whether B7 costimulation can be mediated by a molecule on T cells that is neither CD28 nor CTLA4, we generated mice lacking both of these receptors. CD28/CTLA4(-/-) mice resemble CD28(-/-) mice in having decreased expression of T-cell activation markers in vivo and decreased T-cell proliferation in vitro, as compared with wild-type mice. Using multiple approaches, we find B7-dependent costimulation in CD28/CTLA4(-/-) mice. The proliferation of CD28/CTLA4(-/-) T cells is inhibited by CTLA4-Ig and by the use of antigen-presenting cells lacking both B7-1 and B7-2. CD28/CTLA4(-/-) T-cell proliferation is increased by exposure to Chinese hamster ovary cells transfected with B7-1 or B7-2. Finally, administration of CTLA4-Ig to CD28/CTLA4(-/-) cardiac allograft recipients significantly prolongs graft survival. These data support the existence of an additional receptor for B7 molecules that is neither CD28 nor CTLA4.

摘要

为了研究B7共刺激是否可由T细胞上既非CD28也非CTLA4的分子介导，我们培育出了缺乏这两种受体的小鼠。与野生型小鼠相比，CD28/CTLA4(-/-)小鼠在体内T细胞活化标志物表达降低，体外T细胞增殖减少，这与CD28(-/-)小鼠相似。通过多种方法，我们在CD28/CTLA4(-/-)小鼠中发现了B7依赖性共刺激。CD28/CTLA4(-/-) T细胞的增殖受到CTLA4-Ig以及使用缺乏B7-1和B7-2的抗原呈递细胞的抑制。通过暴露于转染了B7-1或B7-2的中国仓鼠卵巢细胞，CD28/CTLA4(-/-) T细胞的增殖增加。最后，给CD28/CTLA4(-/-)心脏同种异体移植受体施用CTLA4-Ig可显著延长移植物存活时间。这些数据支持存在一种既非CD28也非CTLA4的B7分子额外受体。