抗体之外的 B 细胞在 HBV 诱导的肿瘤发生中的作用:常见变异性免疫缺陷的恶性癌症--临床和免疫移植的意义及文献综述

Diseases Pub Date : 2024-04-23 DOI:10.3390/diseases12050080
P. Zdziarski, Andrzej Gamian
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引用次数: 0

摘要

虽然淋巴瘤是常见可变免疫缺陷病(CVID)中最常见的恶性肿瘤,但实体瘤,尤其是受致癌病毒影响的实体瘤,并没有被考虑在内。此外,体外遗传学研究和细胞培养并不能满足免疫系统与 HBV 相互作用的需要。我们采用了之前引入的宿主与病毒相互作用的临床模型(即免疫缺陷的感染过程)来分析 B 细胞和特异性 IgG 的作用(对一名接受静脉注射免疫球蛋白(IVIG)的 CVID 患者的观察性研究)。患者病情突然恶化,检测出 HBs 和 HBV-DNA 阳性(369 × 106 拷贝)。尽管接受了拉米夫定治疗,IVIG 也从 0.3 克/千克增加到 0.4 克/千克,但 CT 显示肝内肿瘤(肝细胞癌)长达 11 厘米。抗-HBs在延时分析中呈阳性(范围为 111-220 IU/mL)。肾功能衰竭的免疫复合物疾病使替代疗法的强化变得复杂。CVID 中的恶性 HCC 以及作为首发症状的肿瘤发生值得关注。遗憾的是,乙型肝炎免疫球蛋白(HBIG)治疗在移植后维持治疗中起着重要作用。抗乙肝替代治疗尚未被证明有效、具有肿瘤保护作用,也不安全。因此,应谨慎地尽量减少对 HBV 感染受者的免疫抑制,并更精确地选择患者,排除 HBV 阳性供者。我们的临床模型显示了一个具有重要体液宿主因素的 HCC 通路,这与仅强调风险因素(如慢性肝炎)的流行病学/队列研究相反。在 CVID 中观察到的缺乏细胞合作和 B 细胞缺陷在 HBV 大量复制,尤其是致癌过程中起着至关重要的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of B Cells beyond Antibodies in HBV-Induced Oncogenesis: Fulminant Cancer in Common Variable Immunodeficiency—Clinical and Immunotransplant Implications with a Review of the Literature
Although lymphoma is the most frequent malignancy in common variable immunodeficiency (CVID), solid tumors, especially affected by oncogenic viruses, are not considered. Furthermore, in vitro genetic studies and cell cultures are not adequate for immune system and HBV interaction. We adopted a previously introduced clinical model of host–virus interaction (i.e., infectious process in immunodeficiency) for analysis of B cells and the specific IgG role (an observational study of a CVID patient who received intravenous immunoglobulin (IVIG). Suddenly, the patient deteriorated and a positive results of for HBs and HBV-DNA (369 × 106 copies) were detected. Despite lamivudine therapy and IVIG escalation (from 0.3 to 0.4 g/kg), CT showed an 11 cm intrahepatic tumor (hepatocellular carcinoma). Anti-HBs were positive in time-lapse analysis (range 111–220 IU/mL). Replacement therapy intensification was complicated by an immune complex disease with renal failure. Fulminant HCC in CVID and the development of a tumor as the first sign is of interest. Unfortunately, treatment with hepatitis B immune globulins (HBIG) plays a major role in posttransplant maintenance therapy. Anti-HB substitution has not been proven to be effective, oncoprotective, nor safe. Therefore, immunosuppression in HBV-infected recipients should be carefully minimized, and patient selection more precise with the exclusion of HBV-positive donors. Our clinical model showed an HCC pathway with important humoral host factors, contrary to epidemiological/cohort studies highlighting risk factors only (e.g., chronic hepatitis). The lack of cell cooperation as well as B cell deficiency observed in CVID play a crucial role in high HBV replication, especially in carcinogenesis.
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