McAdam A J, Schweitzer A N, Sharpe A H
Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA.
Immunol Rev. 1998 Oct;165:231-47. doi: 10.1111/j.1600-065x.1998.tb01242.x.
The functional significance of B7 co-stimulation in T-cell activation was described first in the context of preventing the induction of anergy. The functions of this pathway are far more complex than initially appreciated in view of the existence of two B7 molecules which have specificities for both CD28 and CTLA-4, which serve to amplify and terminate T-cell responses respectively. Mice lacking B7 co-stimulators and CD28 and CTLA-4 co-stimulatory receptors are helping to clarify the functions of this key immunoregulatory pathway. In this review we will focus on the role of B7 co-stimulation in the activation and differentiation of CD4+ helper cells and CD8+ cytotoxic cells. The contribution of B7 co-stimulation to CD4+ responses depends upon the activation history of the T-cell and the strength of the T-cell antigen receptor signal. B7 co-stimulation contributes to interleukin (IL)-2 production by both naive and previously activated CD4+ T cells. B7 co-stimulation is most critical for the differentiation of naive CD4+ T cells to IL-4 producers, but predominately influences IL-2 production by previously activated CD4+ cells. B7 co-stimulation is important in development of cytotoxic T cells through both effects on T-helper cells and by direct co-stimulation of CD8+ cells.
B7共刺激在T细胞活化中的功能意义最初是在防止无反应性诱导的背景下被描述的。鉴于存在对CD28和CTLA-4均具有特异性的两种B7分子，该途径的功能远比最初认识到的更为复杂，这两种分子分别用于放大和终止T细胞反应。缺乏B7共刺激分子以及CD28和CTLA-4共刺激受体的小鼠有助于阐明这一关键免疫调节途径的功能。在本综述中，我们将重点关注B7共刺激在CD4+辅助性T细胞和CD8+细胞毒性T细胞的活化及分化中的作用。B7共刺激对CD4+反应的贡献取决于T细胞的活化历史以及T细胞抗原受体信号的强度。B7共刺激对幼稚和先前活化的CD4+ T细胞产生白细胞介素（IL）-2均有促进作用。B7共刺激对于幼稚CD4+ T细胞分化为IL-4产生细胞最为关键，但主要影响先前活化的CD4+细胞产生IL-2。B7共刺激通过对辅助性T细胞的作用以及对CD8+细胞的直接共刺激，在细胞毒性T细胞的发育中发挥重要作用。
