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Related Experiment Video

Updated: Dec 25, 2025

Flow-sorting and Exome Sequencing of the Reed-Sternberg Cells of Classical Hodgkin Lymphoma
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[Microenvironment in classical Hodgkin lymphoma].

Anja Mottok1

  • 1Institut für Humangenetik, Universitätsklinikum Ulm, Albert-Einstein-Allee 11, 89081, Ulm, Deutschland. anja.mottok@uni-ulm.de.

Der Pathologe
|April 3, 2020
PubMed
Summary

Classical Hodgkin lymphoma (cHL) pathogenesis involves Hodgkin and Reed-Sternberg (HRS) cells manipulating the immune microenvironment. Genetic factors like 9p24.1 gains and PD-1/PD-L1/PD-L2 interactions are key to immune evasion and treatment response.

Keywords:
Hodgkin- and Reed-Sternberg cellImmune escapePD-1 ligandsPrognostic modelsTumor-associated macrophages

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Area of Science:

  • Oncology
  • Immunology
  • Genetics

Background:

  • Classical Hodgkin lymphoma (cHL) is characterized by a significant immune cell infiltrate.
  • Hodgkin and Reed-Sternberg (HRS) cells actively shape the tumor microenvironment.
  • The composition of the immune infiltrate varies with histological subtype and Epstein-Barr Virus (EBV) status.

Purpose of the Study:

  • To elucidate the mechanisms of immune evasion in cHL pathogenesis.
  • To understand the role of genetic alterations, particularly 9p24.1 locus gains, in cHL.
  • To explore the impact of PD-1/PD-L1/PD-L2 interactions on immune suppression and therapeutic response.

Main Methods:

  • Analysis of genetic studies identifying key oncogenic pathways in cHL.
  • Assessment of immune microenvironment composition in cHL.
  • Correlation of genetic findings, microenvironment, and clinical outcomes.

Main Results:

  • HRS cells escape immune surveillance through mechanisms including impaired antigen presentation and 9p24.1 locus gains.
  • Gains in the 9p24.1 locus lead to increased expression of JAK2, PD-L1, and PD-L2, promoting immune suppression.
  • The reversibility of PD-1 pathway interactions is crucial for the efficacy of checkpoint inhibitors in cHL.

Conclusions:

  • Understanding cHL pathogenesis involves HRS cell-driven immune modulation and genetic alterations.
  • Prognostic models integrating microenvironment and genetic data can improve risk stratification and treatment selection.
  • Targeting immune evasion pathways offers therapeutic opportunities for cHL patients, particularly in relapsed settings.