The Journal of Experimental Medicine
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Published online 31 July 2006 doi:10.1084/jem.20052136
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 8, 1859-1865
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BRIEF DEFINITIVE REPORT

 Enhancement of clonogenicity of human multiple myeloma by dendritic cells

Anjli Kukreja1, Aisha Hutchinson1, Kavita Dhodapkar2, Amitabha Mazumder3, David Vesole3, Revathi Angitapalli1, Sundar Jagannath3, and Madhav V. Dhodapkar1,4

1 Laboratory of Tumor Immunology and Immunotherapy and 2 Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, NY 10021
3 St. Vincent's Cancer Center, New York, NY 10021
4 Hematology Service, Memorial Sloan Kettering Cancer Center, New York, NY 10021

CORRESPONDENCE Madhav V. Dhodapkar: dhodapm{at}rockefeller.edu

Infiltration by dendritic cells (DCs) is a common feature of most human tumors. Prior studies evaluating the interaction of DCs with tumors have focused largely on their immunologic properties (for review see Banchereau, J., and R.M. Steinman. 1998. Nature. 392:245–252). In this study, we show that the clonogenicity of several human tumor cell lines and primary tumor cells from myeloma patients is enhanced by their interactions with DCs. Myeloma cells cultured in the presence of DCs have an altered phenotype with an increased proportion of cells lacking terminal plasma cell differentiation marker CD138. DC–tumor interaction also leads to the up-regulation of B cell lymphoma 6 expression in myeloma cells. Effects of DCs on myeloma cells are inhibited by blockade of the receptor activator of NF-kB (RANK)–RANK ligand and B cell–activating factor–APRIL (a proliferation-inducing ligand)-mediated interactions. Together, these data suggest that tumor–DC interactions may directly impact the biology of human tumors, particularly multiple myeloma, and may be a target for therapeutic intervention.


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