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Prepublished online as a Blood First Edition Paper on April 17, 2002; DOI 10.1182/blood-2002-01-0099.
Submitted January 15, 2002
Accepted February 14, 2002
The role of cytokines in classical Hodgkin lymphoma
Tak W Mak* and Brian F Skinnider
Amgen Research Institute, Toronto, Ontario, Canada; Ontario Cancer Institute, Toronto, Ontario, Canada; Departments of Medical Biophysics and Immunology, University of Toronto, Toronto, Ontario, Canada
* Corresponding author; email: tmak{at}oci.utoronto.ca.
The clinical and pathologic features of classical Hodgkin lymphoma (cHL) reflect an abnormal immune response that is thought to be due to the elaboration of a variety of cytokines by the malignant Reed-Sternberg (RS) cells or surrounding tissues. The majority of cHL cases are characterized by expression of tumor necrosis factor receptor (TNFR) family members and their ligands, as well as an unbalanced production of Th2 cytokines and chemokines. Activation of TNFR members results in constitutive activation of NF B, a transcription factor important for the in vitro and in vivo growth of RS cell lines. The expression of Th2 cytokines and chemokines leads to the reactive infiltrate of eosinophils, Th2 cells and fibroblasts characteristic of cHL, and can also contribute to a local suppression of Th1 cell-mediated cellular immune response. Another particularly important growth and survival factor for RS cell lines is the Th2 cytokine IL-13, which is also commonly expressed by primary RS cells. In approximately 40% of cHL cases, the presence of Epstein-Barr virus influences the Th1/Th2 balance towards the production of Th1 cytokines and chemokines, but this shift is apparently insufficient for the stimulation of an effective anti-tumor cell-mediated immune response. This review will summarize the current literature on cytokine expression by and activity on RS cell lines and primary cHL tissues, examine cytokine signaling pathways in RS cells, and discuss the role that cytokines play in the specific clinical and pathologic features of cHL.
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