经典霍奇金淋巴瘤 (cHL) 是一种高度可治愈的疾病，但约 20% 的患者在标准一线化疗方案后会出现病情进展或复发。自体干细胞移植后的挽救方案代表了这些病例的历史治疗方法。在过去的十年中，随着人们对 cHL 生物学和肿瘤微环境在疾病过程中的作用的日益了解，新的分子已被引入临床实践，改善了复发/难治性治疗的结果。抗 CD30 抗体药物偶联的 brentuximab vedotin 和 PD-1/PD-L1 检查点抑制剂代表了当今化疗难治性患者的治疗选择，最近的随机试验证明了它们在一线免疫化疗联合治疗中的功效。几种能够调节患者 T 淋巴细胞和 NK 细胞活性的药物以及许多抗 CD30 嵌合抗原受体 T 细胞产品正在开发中。多种肿瘤异常表观遗传机制正在被研究作为抗肿瘤化合物（例如组蛋白脱乙酰酶抑制剂和低甲基化剂）的靶标。此外，JAK2 抑制与抗 PD1 阻断相结合揭示了 cHL 中潜在的互补治疗途径。在这篇综述中，我们将总结 cHL 生物学的最新发现和临床上可用的新治疗方案，以及该领域的有前景的未来前景。

Classical Hodgkin Lymphoma (cHL) is a highly curable disease, but around 20% of patients experience progression or relapse after standard frontline chemotherapy regimens. Salvage regimens followed by autologous stem cell transplants represent the historical treatment approach for these cases. In the last decade, with the increasing understanding of cHL biology and tumor microenvironment role in disease course, novel molecules have been introduced in clinical practice, improving outcomes in the relapsed/refractory setting. The anti-CD30 antibody-drug conjugated brentuximab vedotin and PD-1/PD-L1 checkpoint inhibitors represent nowadays curative options for chemorefractory patients, and randomized trials recently demonstrated their efficacy in frontline immune-chemo-combined modalities. Several drugs able to modulate the patients' T-lymphocytes and NK cell activity are under development, as well as many anti-CD30 chimeric antigen receptor T-cell products. Multiple tumor aberrant epigenetic mechanisms are being investigated as targets for antineoplastic compounds such as histone deacetylase inhibitors and hypomethylating agents. Moreover, JAK2 inhibition combined with anti-PD1 blockade revealed a potential complementary therapeutic pathway in cHL. In this review, we will summarize recent findings on cHL biology and novel treatment options clinically available, as well as promising future perspectives in the field.