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CD30 ligand is frequently expressed in human hematopoietic malignancies of
myeloid and lymphoid origin
V Gattei, M Degan, A Gloghini, A De Iuliis, S Improta, FM Rossi, D Aldinucci, V Perin, D Serraino, R Babare, V Zagonel, HJ Gruss, A Carbone and A Pinto
Department of Medical Oncology, Centro di Riferimento Oncologico, INRCCS,
Aviano, Italy.
CD30 ligand (CD30L) is a type-II membrane glycoprotein capable of
transducing signals leading to either cell death or proliferation through
its specific counterstructure CD30. Although several lines of evidence
indicate that CD30L plays a key role as a paracrine- or autocrine-acting
surface molecule in the deregulated cytokine cascade of Hodgkin's disease,
little is known regarding its distribution and biologic significance in
other human hematopoietic malignancies. By analyzing tumor cells from 181
patients with RNA studies and immunostaining by the anti-CD30L monoclonal
antibody M80, we were able to show that human hematopoietic malignancies of
different lineage and maturation stage display a frequent and broad
expression of the ligand. CD30L mRNA and surface protein were detected in
60% of acute myeloid leukemias (AMLs), 54% of B-lineage acute lymphoblastic
leukemias (ALLs), and in a consistent fraction (68%) of B-cell
lymphoproliferative disorders. In this latter group, hairy cell leukemia
and high-grade B-cell non-Hodgkin's lymphoma (B-NHL) expressed a higher
surface density of CD30L as compared with B-cell chronic lymphocytic
leukemia and low-grade B-NHL. Purified plasmacells from a fraction of
multiple myeloma patients also displayed CD30L mRNA and protein. A more
restricted expression of CD30L was found in T-cell tumors that was mainly
confined to neoplasms with an activated peripheral T-cell phenotype, such
as T-cell prolymphocytic leukemia, peripheral T-NHL, and adult T-cell
leukemia/lymphoma. In contrast, none of the T-lineage ALLs analyzed
expressed the ligand. In AML, a high cellular density of CD30L was detected
in French-American-British M3, M4, and M5 phenotypes, which are directly
associated with the presence on tumor cells of certain surface structures,
including the p55 interleukin-2 receptor alpha-chain, the alpha(M) (CD11b)
chain of beta2 integrins, and the intercellular adhesion molecule-1 (CD54).
Analysis of normal hematopoietic cells evidenced that, in addition to
circulating and tonsil B cells, a fraction of bone marrow myeloid
precursors, erythroblasts, and subsets of megakaryocytes also express
CD30L. Finally, we have shown that native CD30L expressed on primary
leukemic cells is functionally active by triggering both mitogenic and
antiproliferative signals on CD30+ target cells. As opposed to CD30L, only
10 of 181 primary tumors expressed CD30 mRNA or protein, rendering
therefore unlikely a CD30-CD30L autocrine loop in human hematopoietic
neoplasms. Taken together, our data indicate that CD30L is widely expressed
from early to late stages of human hematopoiesis and suggest a regulatory
role for this molecule in the interactions of normal and malignant
hematopoietic cells with CD30+ immune effectors and/or microenvironmental
accessory cells.
Volume 89,
Issue 6,
pp. 2048-2059,
03/15/1997
Copyright © 1997 by The American Society of Hematology
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