Janssen R A, Kroesen B J, Buter J, Mesander G, Sleijfer D T, The T H, Mulder N H, de Leij L
Department of Clinical Immunology, University Hospital, Groningen, The Netherlands.
Br J Cancer. 1995 Sep;72(3):795-9. doi: 10.1038/bjc.1995.414.
We report the immunomodulatory effects of an intravenous treatment with F(ab')2 fragments of the bispecific monoclonal antibody BIS-1 during subcutaneous recombinant interleukin 2 (rIL-2) therapy of renal cell cancer (RCC) patients. BIS-1 is directed against both the CD3 antigen on T cells and the EGP-2 molecule on carcinoma cells and some normal epithelia. The amount of BIS-1 F(ab')2 bound to peripheral blood lymphocytes (PBLs) increased dose-dependently. This occupation degree was highest at the end of the 2 h infusion and rapidly decreased subsequently. During the first hour of BIS-1 F(ab')2 infusion the number of PBLs decreased slowly. This was followed by an increase in serum tumour necrosis factor alpha (TNF-alpha) concentrations and a rapid decrease in the numbers of peripheral blood lymphocytes, monocytes and eosinophils. In our view, the most likely explanation for the observed decrease in occupation degree of BIS-1 F(ab')2 and the rise in TNF-alpha levels is based on the assumption that BIS-1-carrying T cells leave the circulation. The CD3 antigens on these extravasated T cells become cross-linked by EGP-2 antigens, inducing TNF-alpha secretion. This results in an enhanced decrease in the numbers of PBLs, monocytes and eosinophils. These preliminary results suggest that BIS-1 F(ab')2 treatment during IL-2 therapy may induce local T-cell activation.
我们报告了在肾细胞癌(RCC)患者皮下重组白细胞介素2(rIL-2)治疗期间,双特异性单克隆抗体BIS-1的F(ab')2片段静脉治疗的免疫调节作用。BIS-1针对T细胞上的CD3抗原以及癌细胞和一些正常上皮细胞上的EGP-2分子。与外周血淋巴细胞(PBL)结合的BIS-1 F(ab')2量呈剂量依赖性增加。这种占据程度在2小时输注结束时最高,随后迅速下降。在BIS-1 F(ab')2输注的第一个小时内,PBL数量缓慢减少。随后血清肿瘤坏死因子α(TNF-α)浓度升高,外周血淋巴细胞、单核细胞和嗜酸性粒细胞数量迅速减少。我们认为,观察到的BIS-1 F(ab')2占据程度降低和TNF-α水平升高的最可能解释是基于携带BIS-1的T细胞离开循环的假设。这些渗出的T细胞上的CD3抗原被EGP-2抗原交联,诱导TNF-α分泌。这导致PBL、单核细胞和嗜酸性粒细胞数量进一步减少。这些初步结果表明,IL-2治疗期间的BIS-1 F(ab')2治疗可能诱导局部T细胞活化。