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首页> 外文期刊>Journal of immunotherapy >Subcutaneous administration of interleukin-2 triggers Fcgamma receptor I expression on human peripheral blood neutrophils in solid and hematologic malignancies.
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Subcutaneous administration of interleukin-2 triggers Fcgamma receptor I expression on human peripheral blood neutrophils in solid and hematologic malignancies.

机译：皮下注射白介素2会触发实体和血液系统恶性肿瘤中人外周血中性粒细胞的Fcγ受体I表达。

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Freshly isolated human polymorphonuclear cells (PMNCs) constitutively express Fcgamma receptor (Fc-gammaR) II and FcgammaRIII on the cell surface but not FcgammaRI. Cytokines such as interferon-gamma (IFNgamma), granulocyte-macrophage colony-stimulating factor (CSF), and granulocyte-CSF trigger FcgammaRI expression on (PMNCs). Because PMNCs express interleukin (IL)-2 receptor, we investigated whether IL-2 can induce FcgammaRI expression on PMNCs isolated from IL-2-treated metastatic renal cell carcinoma (MRCC) and low-grade non-Hodgkin lymphoma (LGNHL) patients. Pretherapy flow cytometry analysis of Fcgamma receptors on PMNCs did not show FcgammaRI expression. Interestingly, 3 days after therapy, PMNCs displayed a detectable amount of FcgammaRI on the cell surface. Kinetic studies on the in vivo effects of IL-2 on MRCC patients showed that FcgammaRI was transiently expressed, starting within 3-6 days of therapy, remaining expressed for 10-15 days, and rapidly declining, whereas such expression remained stable for months in LGNHL patients. In contrast, Fc-gammaRII was not affected. In addition, FcgammaRI+ PMNCs coated in vitro with a bispecific antibody Fab anti-FcgammaRI x anti-HER-2eu formed intercellular conjugates with a human HER-2eu-transfected 3T3 cell line (HER-2eu-3T3). Interleukin-2 treatment increased the number of FcgammaRIII low eosinophils, leading to a change in FcgammaRIII distribution among granulocyte cell subsets. In vitro IL-2 treatment of purified PMNCs failed to generate Fc-gammaRI expression, suggesting that IL-2 indirectly causes FcgammaRI expression. During the IL-2 administration, we did not observe significant changes in IFNgamma serum level. In conclusion, our observation may be used to potentiate the antitumor effects of IL-2 in novel immunotherapy regimens, perhaps by redirecting FcgammaRI+ PMNCs against cancer cells by heteroconjugate antibodies and monitoring the biologic activity of subcutaneous IL-2 in cancer patients.
机译：新鲜分离的人多形核细胞（PMNC）在细胞表面组成性表达Fcgamma受体（Fc-gammaR）II和FcgammaRIII，但不表达FcgammaRI。诸如干扰素-γ（IFNγ），粒细胞-巨噬细胞集落刺激因子（CSF）和粒细胞-CSF的细胞因子触发FcgammaRI表达（PMNC）。因为PMNCs表达白介素（IL）-2受体，所以我们调查了IL-2是否能诱导IL-2治疗从经IL-2治疗的转移性肾细胞癌（MRCC）和低度非霍奇金淋巴瘤（LGNHL）患者中分离出的PMNC上FcgammaRI表达。 PMNC上Fcgamma受体的治疗前流式细胞术分析未显示FcgammaRI表达。有趣的是，治疗后3天，PMNC在细胞表面显示出可检测量的FcgammaRI。关于IL-2对MRCC患者的体内作用的动力学研究表明，FcgammaRI瞬时表达，从治疗3-6天开始，持续表达10-15天，然后迅速下降，而这种表达在几个月内保持稳定。 LGNHL患者。相反，Fc-γRII不受影响。另外，在体外用双特异性抗体Fab抗-FcgammaRI x抗-HER-2 / neu包被的FcgammaRI + PMNC与人HER-2 / neu转染的3T3细胞系（HER-2 / neu-3T3）形成了细胞间结合物。白介素2处理增加了FcgammaRIII低嗜酸性粒细胞的数量，导致粒细胞亚群中FcgammaRIII分布的改变。纯化PMNC的体外IL-2处理无法产生Fc-gammaRI表达，表明IL-2间接引起FcgammaRI表达。在IL-2给药期间，我们没有观察到IFNgamma血清水平的明显变化。总之，我们的观察结果可用于增强IL-2在新型免疫治疗方案中的抗肿瘤作用，也许是通过杂合结合抗体重定向FcgammaRI + PMNC对癌细胞的作用并监测皮下IL-2在癌症患者中的生物学活性。

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