Norton S D, Zuckerman L, Urdahl K B, Shefner R, Miller J, Jenkins M K
Department of Microbiology, University of Minnesota Medical School, Minneapolis 55455.
J Immunol. 1992 Sep 1;149(5):1556-61.
Previous studies demonstrated that a human pre-B acute lymphoblastic leukemia cell line, NALM-6, failed to stimulate a primary MLR, despite expression of class II MHC and adhesion molecules. Here we demonstrate that this is the result of the fact that NALM-6 cells do not express the ligand for CD28, namely B7. NALM-6 transfectants that expressed high levels of B7 gained the capacity to stimulate IL-2 production by class II MHC molecule-specific alloreactive T cells and to costimulate a polyclonal population of purified T cells cultured with immobilized anti-CD3 mAb. In the presence of PMA, NALM-6 cells transfected with B7 polyclonally stimulated T cells in a cyclosporine A-resistant fashion, a property previously attributed only to agonistic anti-CD28 mAb. The gain of these functions could not be explained solely by an increased capacity of the transfectants to form conjugates with T cells, suggesting that the CD28/B7 interaction transduces a costimulatory signal in T cells.
先前的研究表明，一种人类前B细胞急性淋巴细胞白血病细胞系NALM-6，尽管表达II类主要组织相容性复合体（MHC）和黏附分子，但未能刺激原发性混合淋巴细胞反应（MLR）。在此我们证明，这是由于NALM-6细胞不表达CD28的配体，即B7这一事实所致。表达高水平B7的NALM-6转染子获得了刺激II类MHC分子特异性同种异体反应性T细胞产生白细胞介素-2（IL-2）的能力，以及共刺激用固定化抗CD3单克隆抗体培养的纯化T细胞多克隆群体的能力。在佛波酯（PMA）存在的情况下，用B7转染的NALM-6细胞以环孢素A抗性方式多克隆刺激T细胞，这一特性以前仅归因于激动性抗CD28单克隆抗体。这些功能的获得不能仅通过转染子与T细胞形成结合物能力的增加来解释，这表明CD28/B7相互作用在T细胞中传导共刺激信号。
