CHARACTERIZATION OF INTERLEUKIN-2 RECEPTORS ON B-CELL CHRONIC LYMPHOCYTIC-LEUKEMIA CELLS

Citation
V. Tsilivakos et al., CHARACTERIZATION OF INTERLEUKIN-2 RECEPTORS ON B-CELL CHRONIC LYMPHOCYTIC-LEUKEMIA CELLS, Leukemia, 8(9), 1994, pp. 1571-1578
Citations number
28
Categorie Soggetti
Hematology,Oncology
Journal title
ISSN journal
08876924
Volume
8
Issue
9
Year of publication
1994
Pages
1571 - 1578
Database
ISI
SICI code
0887-6924(1994)8:9<1571:COIROB>2.0.ZU;2-8
Abstract
The expression and function of IL-2R chains expressed on B-cell chroni c lymphocytic leukemia (B-CLL) cells were analyzed. lL-2R alpha was ex pressed in 31 out of 34 studied cases; in 17 cases more than 50% of th e cells were positive whereas in three cases the proportion of IL-2R a lpha(+) cells was less than 10%. In two patients, 6 and 13% of the cel ls were IL-2R beta(+), in six other cases only 2-3% of the B-CLL cells could be stained with the TU27 moAb whereas in all other cases no pos itive cells could be detected. Equilibrium binding experiments using I -125-rIL2 revealed high (seven out of 15 studied cases), intermediate (four out of 15 cases) and low (five out of 15 cases) affinity IL-2R. The number of high and intermediate affinity IL-2R was low (range: 145 -800 and 40-2800 binding sites/cells, respectively). In all cases inve stigated, both IL-2R alpha and IL-2R beta chain mRNA could be detected , although their quantity was variable from patient to patient. Exogen ous recombinant IL-2 induced, in a dose-response manner, cell prolifer ation in ten out of 23 cases and this effect was independent of the ex pression of IL-2R alpha; however, only cells expressing high affinity IL-2R could respond to exogenous rIL-2. Moreover, anti-IL-2R alpha moA b could inhibit both spontaneous (in three out of five cases) and IL-2 -induced (in five out of five cases) B-CLL cell proliferation. These f indings demonstrate that in a subgroup of B-CLL, leukemic cells are de pendent on the IL-2/IL-2R system whereas in another group, although ce lls expressed functional IL-2 binding sites, they could not respond to the mitogenic signal of IL-2.