Weinberg A D, Rivera M M, Prell R, Morris A, Ramstad T, Vetto J T, Urba W J, Alvord G, Bunce C, Shields J
Earle A. Chiles Research Institute, Robert W. Franz Cancer Research Center, Providence Portland Medical Center, Portland, OR 97213, USA.
J Immunol. 2000 Feb 15;164(4):2160-9. doi: 10.4049/jimmunol.164.4.2160.
The OX-40 receptor (OX-40R), a member of the TNFR family, is primarily expressed on activated CD4+ T lymphocytes. Engagement of the OX-40R, with either OX-40 ligand (OX-40L) or an Ab agonist, delivers a strong costimulatory signal to effector T cells. OX-40R+ T cells isolated from inflammatory lesions in the CNS of animals with experimental autoimmune encephalomyelitis are the cells that respond to autoantigen (myelin basic protein) in vivo. We identified OX-40R+ T cells within primary tumors and tumor-invaded lymph nodes of patients with cancer and hypothesized that they are the tumor-Ag-specific T cells. Therefore, we investigated whether engagement of the OX-40R in vivo during tumor priming would enhance a tumor-specific T cell response. Injection of OX-40L:Ig or anti-OX-40R in vivo during tumor priming resulted in a significant improvement in the percentage of tumor-free survivors (20-55%) in four different murine tumors derived from four separate tissues. This anti-OX-40R effect was dose dependent and accentuated tumor-specific T cell memory. The data suggest that engagement of the OX-40R in vivo augments tumor-specific priming by stimulating/expanding the natural repertoire of the host's tumor-specific CD4+ T cells. The identification of OX-40R+ T cells clustered around human tumor cells in vivo suggests that engagement of the OX-40R may be a practical approach for expanding tumor-reactive T cells and thereby a method to improve tumor immunotherapy in patients with cancer.
OX-40受体(OX-40R)是肿瘤坏死因子受体(TNFR)家族的成员之一,主要表达于活化的CD4+ T淋巴细胞上。OX-40R与OX-40配体(OX-40L)或抗体激动剂结合,可向效应T细胞传递强烈的共刺激信号。从患有实验性自身免疫性脑脊髓炎动物的中枢神经系统炎性病变中分离出的OX-40R+ T细胞,是体内对自身抗原(髓鞘碱性蛋白)产生反应的细胞。我们在癌症患者的原发性肿瘤和肿瘤侵袭的淋巴结中鉴定出了OX-40R+ T细胞,并推测它们是肿瘤抗原特异性T细胞。因此,我们研究了在肿瘤启动过程中体内OX-40R的结合是否会增强肿瘤特异性T细胞反应。在肿瘤启动期间于体内注射OX-40L:Ig或抗OX-40R,可使来自四个不同组织的四种不同小鼠肿瘤的无瘤存活者百分比显著提高(20%-55%)。这种抗OX-40R效应具有剂量依赖性,并增强了肿瘤特异性T细胞记忆。数据表明,体内OX-40R的结合通过刺激/扩增宿主肿瘤特异性CD4+ T细胞的天然库,增强了肿瘤特异性启动。体内在人肿瘤细胞周围聚集的OX-40R+ T细胞的鉴定表明,OX-40R的结合可能是一种扩增肿瘤反应性T细胞的实用方法,从而是一种改善癌症患者肿瘤免疫治疗的方法。