Lenschow D J, Bluestone J A
Ben May Institute, Department of Pathology and the Committee on Immunology, University of Chicago, Illinois 60637.
Curr Opin Immunol. 1993 Oct;5(5):747-52. doi: 10.1016/0952-7915(93)90132-c.
Previous studies have shown that effective T-cell activation requires the engagement of the T-cell receptor complex with MHC-peptide, in parallel with co-stimulation via cell surface adhesion molecules. Blocking these co-stimulatory interactions, in particular the signal transduction via the CD28 molecule, inhibits T-cell activation in vitro and induces T-cell clones into a state of unresponsiveness, termed T-cell anergy. Recent studies have examined the therapeutic effects of treating mice with CD28-B7 antagonists and highlighted the complexity of the CD28 co-stimulatory pathway, as illustrated by the finding that multiple cross-binding ligands for the CD28 and B7 molecules exist that may differentially regulate immune responses.
先前的研究表明，有效的T细胞活化需要T细胞受体复合物与MHC-肽结合，同时通过细胞表面粘附分子进行共刺激。阻断这些共刺激相互作用，特别是通过CD28分子的信号转导，可在体外抑制T细胞活化，并诱导T细胞克隆进入无反应状态，即T细胞无能。最近的研究检测了用CD28-B7拮抗剂治疗小鼠的治疗效果，并强调了CD28共刺激途径的复杂性，这一复杂性体现在发现存在多种CD28和B7分子的交叉结合配体，它们可能对免疫反应有不同的调节作用。
