Freeman G J, Borriello F, Hodes R J, Reiser H, Hathcock K S, Laszlo G, McKnight A J, Kim J, Du L, Lombard D B
Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Boston, MA.
Science. 1993 Nov 5;262(5135):907-9. doi: 10.1126/science.7694362.
B7 delivers a costimulatory signal through CD28, resulting in interleukin-2 secretion and T cell proliferation. Blockade of this pathway results in T cell anergy. The in vivo role of B7 was evaluated with B7-deficient mice. These mice had a 70 percent decrease in costimulation of the response to alloantigen. Despite lacking B7 expression, activated B cells from these mice bound CTLA-4 and GL1 monoclonal antibody, demonstrating that alternative CTLA-4 ligand or ligands exist. These receptors are functionally important because the residual allogenic mixed lymphocyte responses were blocked by CTLA4Ig. Characterization of these CTLA-4 ligands should lead to strategies for manipulating the immune response.
B7通过CD28传递共刺激信号，导致白细胞介素-2分泌和T细胞增殖。阻断该途径会导致T细胞无反应性。利用B7缺陷小鼠评估了B7在体内的作用。这些小鼠对同种异体抗原反应的共刺激减少了70%。尽管缺乏B7表达，但来自这些小鼠的活化B细胞能结合CTLA-4和GL1单克隆抗体，表明存在替代的CTLA-4配体。这些受体在功能上很重要，因为残余的同种异体混合淋巴细胞反应被CTLA4Ig阻断。对这些CTLA-4配体的特性进行表征应能带来操纵免疫反应的策略。
