CD30 ligand (CD30L)-expressing acute myeloid leukemias: a new model of paracrine interactions for the regulation of blast cells proliferation

Citation
V. Gattei et al., CD30 ligand (CD30L)-expressing acute myeloid leukemias: a new model of paracrine interactions for the regulation of blast cells proliferation, LEUK LYMPH, 35(1-2), 1999, pp. 21-35
Citations number
92
Categorie Soggetti
Hematology,"Onconogenesis & Cancer Research
Journal title
LEUKEMIA & LYMPHOMA
ISSN journal
10428194 → ACNP
Volume
35
Issue
1-2
Year of publication
1999
Pages
21 - 35
Database
ISI
SICI code
1042-8194(199909)35:1-2<21:CL(AML>2.0.ZU;2-V
Abstract
CD30 ligand (CD30L) is a type-II membrane glycoprotein capable of transduci ng signals through its specific counterstructure CD30. Even though there ar e indications that CD30L plays a key role as a paracrine-acting surface mol ecule in the deregulated cytokine cascade of Hodgkin's disease, little is k nown about its biological functions in other human hemopoietic malignancies , despite the demonstration of the frequent expression of CD30L in hemopoie tic neoplasms of both myeloid and lymphoid origin. The present review summa rises structural and biological properties of CD30L, and focuses on CD30L() acute myeloid leukemias (AMLs) by recapitulating some phenotypic and clin ical features of this subset of acute leukemias. We also discuss some mecha nisms by which CD30L-expressing leukemic blasts may gain a proliferative ad vantage through direct interaction with specific cells, in turn expressing its specific counterreceptor CD30. In particular, data has been provided su ggesting that CD30L(+)AMLs may evoke a sort of polarized T-cell response wi th the preferential production of Th2-like cytokines, mainly IL-4, by speci fic CD30-expressing T cell subsets. On the other hand, leukemic blasts pres enting surface CD30L, have been shown to express a peculiar cytokine-recept ors pattern that makes them an ideal target for T cells-produced Th2-like c ytokines. Furthermore, some Th2-like cytokines, such as IL-4, are able to e nhance blast cells proliferation, as well as to up-regulate the surface exp ression of specific adhesion molecules that have been shown to be associate d with the presence of CD30L on AML blasts.