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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Pathobiology of classical Hodgkin lymphoma.
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Pathobiology of classical Hodgkin lymphoma.

机译：经典霍奇金淋巴瘤的病理生物学。

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The World Health Organization has acknowledged the malignant nature of classical Hodgkin lymphoma (cHL), which encompasses four histological subtypes. The diagnosis of cHL is based on the detection of malignant Hodgkin and Reed-Sternberg cells (HRSC) confirmed by immunophenotyping and the detection of growth patterns specific to each histological subtype. The pathologic HRSC arise from germinal center or immediate postgerminal cells that lack detectable immunoglobulin/B-cell antigen receptor expression, with a consequent loss of B-cell identity; very few cHL cases are of T-cell origin. To escape apoptosis, which normally occurs in B cells with nonfunctioning antigen receptor machinery, HRSC develop concurrent antiapoptotic mechanisms by activation of nuclear factor-kappaB or are rescued by Epstein-Barr virus infection. HRSC are characterized by a variable and inconstant immunophenotype, with a remarkable loss of lineage-specific cell antigens and expression of antigens of other cell lineages. The master plan of B-cell identity in HRSC is disturbed not only at the immunoglobulin expression level, but also at the transcriptional factor level. HRSC are further characterized by profound cell cycle deregulation with futile replication, multinucleation and poly- and aneuploidy. Here, we review pathobiological aspects of cHL with respect to lymphomagenesis and routine diagnostics.
机译：世界卫生组织已确认经典霍奇金淋巴瘤（cHL）的恶性性质，其中包括四种组织学亚型。 cHL的诊断基于通过免疫表型确定的恶性霍奇金细胞和Reed-Sternberg细胞（HRSC）的检测以及每种组织学亚型特异性生长模式的检测。病理性HRSC来自生发中心或生后即刻的细胞，这些细胞缺乏可检测的免疫球蛋白/ B细胞抗原受体表达，从而丧失了B细胞的特性。很少有cHL病例来自T细胞。为了逃避通常发生在具有非功能性抗原受体机制的B细胞中的凋亡，HRSC通过激活核因子-κB形成并发的抗凋亡机制，或者通过爱泼斯坦-巴尔病毒感染进行挽救。 HRSC的特点是免疫表型可变且不稳定，谱系特异性细胞抗原的显着丧失以及其他细胞谱系的抗原表达。 HRSC中B细胞同一性的总体规划不仅在免疫球蛋白表达水平受到干扰，在转录因子水平也受到干扰。 HRSC的进一步特征是细胞周期失调，复制无效，多核化以及多倍体和非整倍性。在这里，我们回顾了与淋巴瘤的发生和常规诊断有关的cHL的病理生物学方面。

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