Primary immunodeficiencies (PIDs) and secondary immunodeficiencies (SIDs) are characterized by compromised immune function, rendering individuals susceptible to infections and potentially influencing cancer development. Epstein–Barr virus (EBV), a widespread herpesvirus, has been linked to cancer, particularly in those with weakened immune systems. This study aims to compare selected immune parameters, focusing on immune checkpoint molecules (PD-1/PD-L1, CTLA-4/CD86, CD200R/CD200), and EBV reactivation in patients with chronic lymphocytic leukemia (CLL, a representative of SIDs) and common variable immunodeficiency (CVID, a representative of PIDs). We performed a correlation analysis involving patients diagnosed with CLL, CVID, and a healthy control group. EBV reactivation was assessed using specific antibody serology and viral load quantification. Peripheral blood morphology, biochemistry, and immunophenotyping were performed, with emphasis on T and B lymphocytes expressing immune checkpoints and their serum concentrations. Our findings revealed elevated EBV reactivation markers in both CLL and CVID patients compared with healthy controls, indicating increased viral activity in immunodeficient individuals. Furthermore, immune checkpoint expression analysis demonstrated significantly altered percentages of T and B lymphocytes expressing PD-1/PD-L1, CTLA-4/CD86, and CD200R/CD200 in CLL and CVID patients. This suggests a potential interplay between immune checkpoint dysregulation and EBV reactivation in the context of immunodeficiency. In conclusion, our study underscores the intricate relationship between immune dysfunction, EBV reactivation, and immune checkpoint modulation in the context of immunodeficiency-associated cancers. The altered expression of immune checkpoints, along with heightened EBV reactivation, suggests a potential mechanism for immune evasion and tumor progression. These findings provide insights into the complex interactions that contribute to cancer development in immunocompromised individuals, shedding light on potential therapeutic targets for improved management and treatment outcomes. Further investigations are warranted to elucidate the underlying mechanisms and to explore potential interventions to mitigate cancer risk in these patient populations.
原发性免疫缺陷病（PIDs）与继发性免疫缺陷病（SIDs）以免疫功能受损为特征，导致个体易受感染，并可能影响癌症的发生。爱泼斯坦-巴尔病毒（EBV）作为一种广泛存在的疱疹病毒，已被证实与癌症相关，尤其在免疫系统功能低下的人群中。本研究旨在比较慢性淋巴细胞白血病（CLL，作为SIDs的代表）和常见变异型免疫缺陷病（CVID，作为PIDs的代表）患者中选定的免疫参数（重点关注免疫检查点分子PD-1/PD-L1、CTLA-4/CD86、CD200R/CD200）以及EBV再激活情况。我们对诊断为CLL、CVID的患者及健康对照组进行了相关性分析。通过特异性抗体血清学检测和病毒载量定量评估EBV再激活水平。同时进行了外周血形态学、生化学和免疫表型分析，重点关注表达免疫检查点的T淋巴细胞和B淋巴细胞及其血清浓度。研究结果显示，与健康对照组相比，CLL和CVID患者的EBV再激活标志物均升高，表明免疫缺陷个体中病毒活动性增强。此外，免疫检查点表达分析显示，CLL和CVID患者中表达PD-1/PD-L1、CTLA-4/CD86和CD200R/CD200的T、B淋巴细胞百分比发生显著改变。这表明在免疫缺陷背景下，免疫检查点失调与EBV再激活之间可能存在相互作用。综上所述，本研究强调了免疫缺陷相关癌症中免疫功能障碍、EBV再激活与免疫检查点调节之间复杂的关联。免疫检查点的异常表达以及EBV再激活的增强，提示了免疫逃逸和肿瘤进展的潜在机制。这些发现为理解免疫功能低下个体癌症发展的复杂相互作用提供了见解，并为改善治疗管理和疗效的潜在治疗靶点提供了线索。未来需要进一步研究以阐明其潜在机制，并探索降低此类患者群体癌症风险的干预措施。
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