机体特异性免疫应答是一个需要一系列免疫细胞和免疫分子共同参与的异常复杂的过程，这些免疫细胞及分子之间相互调节又相互制约。目前大多数肾脏疾病发病机制尚不明确。B7(CD80)位于调节CD4n +和CD8n +T细胞的抗原提呈细胞上，通过与细胞上的糖蛋白CD28结合发挥信号传递作用、增强或放大免疫反应的功能，或者与细胞毒性T细胞蛋白-4(cytotoxic T lymphocyte-associated antigen4 CTLA-4)结合后抑制免疫应答。通常肾组织不表达或低表达B7，然而某些肾小球疾病的发生与B7的增加有关，其降低了足细胞附着肾小球基底膜的能力，增加炎症反应及肾脏纤维化。当B7与CTLA-4相结合时，免疫反应就会被减弱。因此通过阻断CD28或增强CTLA-4信号可能阻止疾病的发生。该文就共刺激分子B7/CD28在足细胞损伤、原发性肾小球肾炎、紫癜性肾炎、狼疮性肾炎等肾脏疾病的发病机制中的作用，以及B7阻滞剂在部分肾脏疾病靶向治疗的研究进展进行综述。n “,”The body′s specific immune response is a very complicated process involving a series of immune cells and molecules that regulate and restrict each other.At present, the pathogenesis of most kidney diseases is not clear.B7(CD80)is located on antigen-presenting cells that regulate CD4+ and CD8+ T cells and play a role in enhancing or amplifying immune responses by binding to the cellular glycoprotein CD28.It also binds to cytotoxic T lymphocyte-Antigen4(CTLA-4)to inhibit the immune response.In general, renal tissue has no or low expression of B7.However, some glomerular diseases are associated with increased B7, which reduces the ability of podocytes to attach to the glomerular basement membrane and increases inflammation and renal fibrosis.When the B7-CTLA-4 interaction occurs, the immune response is attenuated.The disease can be prevented by blocking CD28 or enhancing the CTLA-4 signal.This article reviewed the role of costimulatory molecule B7/CD28 in the pathogenesis of kidney diseases, such as pod-cell damage, primary glomerulonephritis, purpura nephritis, lupus nephritis.Furthermore, it discussed the feasibility of B7 blockers were used as targeted therapies for kidney diseases.