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Prepublished online as a Blood First Edition Paper on April 17, 2002; DOI 10.1182/blood-2002-01-0099.
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Blood, 15 June 2002, Vol. 99, No. 12, pp. 4283-4297
REVIEW ARTICLE
The role of cytokines in classical Hodgkin lymphoma
Brian F. Skinnider and
Tak
W. Mak
From the Amgen Research Institute, Ontario Cancer
Institute, the Departments of Medical Biophysics and Immunology,
University of Toronto, Ontario, Canada.
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 nuclear factor- B (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 interleukin 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 toward the production of
Th1 cytokines and chemokines, but this shift is apparently insufficient
for the stimulation of an effective antitumor cell-mediated immune
response. This review summarizes the current literature on cytokine
expression by and activity on RS cell lines and primary cHL tissues,
examines cytokine signaling pathways in RS cells, and discusses the
role that cytokines play in the specific clinical and pathologic
features of cHL.
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