open access

Vol 2, No 1 (2011)
Review paper
Published online: 2011-03-24
Get Citation

Reed-Sternberg cell microenvironment in classical Hodgkin lymphoma — pathogenetic role and therapeutic target

Przemysław Juszczyński
Hematologia 2011;2(1):1-14.

open access

Vol 2, No 1 (2011)
REVIEW ARTICLES
Published online: 2011-03-24

Abstract

Classical Hodgkin lymphoma (cHL) is characterized by pathognomonic Reed-Sternberg (R-S) cells, surrounded by an extensive infiltrate of T- and B-lymphocytes, granulocytes, macrophages, plasma cells, eosinophils, mast cells and fibroblasts. This peculiar infiltrate exhibits profound local immunosuppressive properties and extensive network of mutual connections with R-S cells. Chemokines, cytokines and immunomodulatory proteins produced and released by R-S cells directly skew T-cell compartment toward Th2 and Treg cells, and induce infiltration of other cellular components that support R-S cell proliferation. Microenvironment-induced activation of R-S cell surface tumor necrosis factor-family receptors, cytokine receptors and Notch-1 signaling trigger activation of transcription nuclear factor kB (NFkB), JAK–STAT axis and suppression of B-cell transcriptional program. Understanding of these complex relationships led to conceptual design of targeted therapeutic interventions that by selective inhibition of receptor signaling, depletion of microenvironment cellular components or immunomo-dulation can deprive R-S cells from their supportive niche and complement conventional chemotherapy or R-S-cell-targeted drugs. The presented manuscript summarizes current views on the role of microenvironment in cHL, emphasizes its potential therapeutic applications.
Hematologia 2011; 2, 1: 1–14

Abstract

Classical Hodgkin lymphoma (cHL) is characterized by pathognomonic Reed-Sternberg (R-S) cells, surrounded by an extensive infiltrate of T- and B-lymphocytes, granulocytes, macrophages, plasma cells, eosinophils, mast cells and fibroblasts. This peculiar infiltrate exhibits profound local immunosuppressive properties and extensive network of mutual connections with R-S cells. Chemokines, cytokines and immunomodulatory proteins produced and released by R-S cells directly skew T-cell compartment toward Th2 and Treg cells, and induce infiltration of other cellular components that support R-S cell proliferation. Microenvironment-induced activation of R-S cell surface tumor necrosis factor-family receptors, cytokine receptors and Notch-1 signaling trigger activation of transcription nuclear factor kB (NFkB), JAK–STAT axis and suppression of B-cell transcriptional program. Understanding of these complex relationships led to conceptual design of targeted therapeutic interventions that by selective inhibition of receptor signaling, depletion of microenvironment cellular components or immunomo-dulation can deprive R-S cells from their supportive niche and complement conventional chemotherapy or R-S-cell-targeted drugs. The presented manuscript summarizes current views on the role of microenvironment in cHL, emphasizes its potential therapeutic applications.
Hematologia 2011; 2, 1: 1–14
Get Citation

Keywords

classical Hodgkin lymphoma; tumor microenvironment; R-S cell interactions; immune escape; therapeutic targets

About this article
Title

Reed-Sternberg cell microenvironment in classical Hodgkin lymphoma — pathogenetic role and therapeutic target

Journal

Hematology in Clinical Practice

Issue

Vol 2, No 1 (2011)

Article type

Review paper

Pages

1-14

Published online

2011-03-24

Bibliographic record

Hematologia 2011;2(1):1-14.

Keywords

classical Hodgkin lymphoma
tumor microenvironment
R-S cell interactions
immune escape
therapeutic targets

Authors

Przemysław Juszczyński

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.