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Blood, 1 November 2001, Vol. 98, No. 9, pp. 2784-2790
NEOPLASIA
Functional expression of receptor activator of nuclear factor
 B in Hodgkin disease cell lines
Paolo Fiumara,
Virginia Snell,
Yang Li,
Asok Mukhopadhyay,
Mamoun Younes,
Ann Marie Gillenwater,
Fernando Cabanillas,
Bharat B. Aggarwal, and
Anas Younes
From the Departments of Lymphoma and Myeloma, Head and
Neck Surgery, and Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, and the Department of Pathology, Baylor College
of Medicine, Houston, TX.
The malignant Hodgkin and Reed-Sternberg (H/RS) cells of Hodgkin
disease (HD) express several members of the tumor necrosis factor (TNF)
receptor family, including CD30 and CD40, and secrete several cytokines
and chemokines. However, little is known about what regulates cytokine
and chemokine secretion in H/RS cells. Although H/RS cells are
predominantly of B-cell origin, they frequently share phenotypic and
functional features with dendritic cells (DCs). Previous studies
reported that receptor activator of nuclear factor  B
(NF-B) (RANK), a member of the TNF receptor family, is expressed on
DCs, and that RANK ligand (RANKL) enhances DC survival and induces them
to secrete cytokines. This study reports that, similar to DCs, cultured
H/RS cells expressed RANK. However, unlike DCs, H/RS cells also
expressed RANKL. Soluble RANKL activated NF-B and induced messenger
RNA expression of interferon- , interleukin-8 (IL-8), IL-13, IL-9,
IL-15, and RANTES, in addition to the receptors for IL-9, IL-13,
IL-15, and CCR4. RANKL increased IL-8 and IL-13 levels in the
supernatants of H/RS cell lines, an effect that was blocked by soluble
RANK. Furthermore, soluble RANK decreased the basal level of IL-8 in
one cell line, suggesting that IL-8 was induced by an autocrine
RANKL/RANK loop. RANKL had no effect on H/RS cell survival in culture,
and it did not modulate the expression of bcl-2, bcl-xL, bax, or
inhibitors of apoptosis proteins. These data provide evidence of
further functional similarities between DCs and H/RS cells. The
coexpression of RANK and RANKL in H/RS cells suggests that they may
regulate cytokine and chemokine secretion in H/RS cells by an autocrine mechanism.
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