COSTIMULATION OF ANTITUMOR IMMUNITY BY THE B7 COUNTERRECEPTOR FOR THE LYMPHOCYTE-T MOLECULES CD28 AND CTLA-4
COSTIMULATION OF ANTITUMOR IMMUNITY BY THE B7 COUNTERRECEPTOR FOR THE LYMPHOCYTE-T MOLECULES CD28 AND CTLA-4
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DOI：
10.1016/s0092-8674(05)80059-5
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发表时间：
1992-12-24
期刊：
影响因子：
64.5
通讯作者：
LINSLEY, PS
中科院分区：
文献类型：
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作者：
CHEN, LP;ASHE, S;LINSLEY, PS
抗原呈递细胞上的B7分子与T细胞上的受体CD28和CTLA-4相互作用，为T细胞活化提供共刺激信号。我们研究了B7对小鼠黑色素瘤抗肿瘤免疫的影响，该黑色素瘤表达与人乳头瘤病毒E7基因产物相关的排斥抗原。当这种E7+肿瘤在免疫能力强的宿主体内逐渐生长时，用B7共转染其细胞可通过CD8+溶细胞T淋巴细胞介导的B7依赖性免疫反应导致肿瘤消退。E7+B7+肿瘤细胞诱导的免疫应答也可引起E7+B7-肿瘤在远处的消退，并可治愈已建立的E7+B7-微转移。我们的研究结果表明，通过CD28和CTLA-4受体增加T细胞的共刺激可能对产生针对表达病毒抗原的肿瘤的免疫具有治疗作用。
Interaction of the B7 molecule on antigen-presenting cells with its receptors CD28 and CTLA-4 on T cells provides costimulatory signals for T cell activation. We have studied the effects of B7 on antitumor immunity to a murine melanoma that expresses a rejection antigen associated with the E7 gene product of human papillomavirus 16. While this E7+ tumor grows progressively in immunocompetent hosts, cotransfection of its cells with B7 led to tumor regression by a B7-dependent immune response mediated by CD8+ cytolytic T lymphocytes. The immune response induced by E7+B7+ tumor cells also caused regression of E7+B7-tumors at distant sites and was curative for established E7+B7- micrometastases. Our findings suggest that increasing T cell costimulation through the CD28 and CTLA-4 receptors may have therapeutic usefulness for generating immunity against tumors expressing viral antigens.