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(American Journal of Pathology. 2002;160:585-596.)
© 2002 American Society for Investigative Pathology

Regular Articles

Expression of Functional Interleukin-3 Receptors on Hodgkin and Reed-Sternberg Cells

Donatella Aldinucci*, Dalisa Poletto*, Annunziata Gloghini*, Paola Nanni*, Massimo Degan*, Tiziana Perin{dagger}, Paola Ceolin{dagger}, Francesca Maria Rossi*, Valter Gattei*, Antonino Carbone{dagger} and Antonio Pinto*

From the Clinical & Experimental Hematology Research Unit*
and the Division of Pathology,{dagger}
Centro diRiferimento Oncologico, Istituto di Ricovero e Cura a CarattereScientifico, Istituto Nazionale Tumori, Aviano, Italy

The human interleukin-3 receptor (IL-3R) is a heterodimeric complex consisting of an IL-3-specific {alpha} chain (IL-3R{alpha}) and a common ß chain (ßc), this latter shared with the receptors for granulocyte-macrophage colony-stimulating factor and IL-5. Despite extensive research on cytokine circuitries regulating proliferation and survival of tumor cells in Hodgkin’s disease (HD) the functional expression of IL-3Rs in this pathobiological entity has not yet been investigated. In the present study, we demonstrate that the great majority (>90%) of malignant Hodgkin and Reed-Sternberg cells of classic HD (19 of 19 analyzed cases) express IL-3R{alpha} by immunostaining of frozen sections and cell suspensions from involved lymph nodes. Accordingly, HD cell lines (L428, KMH2, HDLM2, L1236) expressed the {alpha} and ß chains of IL-3R both at the mRNA and protein level, with a molecular size of IL-3R{alpha} identical (70 kd) to that expressed by human myeloid cells. Exogenous IL-3 promoted the growth of cultured Hodgkin and Reed-Sternberg cells, such effect being potentiated by IL-9 co-stimulation, and was able to partially rescue tumor cells from apoptosis induced by serum deprivation. This data suggests an involvement of IL-3/IL-3R interactions in the cellular growth of HD through paracrine mechanisms.




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