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Research Article Free access | 10.1172/JCI116042

Interleukin 4 inhibits in vitro proliferation of leukemic and normal human B cell precursors.

D Pandrau, S Saeland, V Duvert, I Durand, A M Manel, M T Zabot, N Philippe, and J Banchereau

Laboratory for Immunological Research, Schering-Plough, Dardilly, France.

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Laboratory for Immunological Research, Schering-Plough, Dardilly, France.

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Laboratory for Immunological Research, Schering-Plough, Dardilly, France.

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Laboratory for Immunological Research, Schering-Plough, Dardilly, France.

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Laboratory for Immunological Research, Schering-Plough, Dardilly, France.

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Published November 1, 1992 - More info

Published in Volume 90, Issue 5 on November 1, 1992
J Clin Invest. 1992;90(5):1697–1706. https://doi.org/10.1172/JCI116042.
© 1992 The American Society for Clinical Investigation
Published November 1, 1992 - Version history
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Abstract

In the present study, we have investigated the effects of IL-4 on the proliferation and differentiation of leukemic and normal human B cell precursors (BCP). We have demonstrated that IL-4 significantly inhibited spontaneous [3H]thymidine ([3H]-TdR) incorporation by leukemic blasts from some B lineage acute lymphoblastic leukemia (BCP-ALL) patients (8 of 14). Furthermore, IL-4 was found to suppress the spontaneous and factor-dependent (IL-7 and IL-3) proliferation of normal BCP (CD10+ surface [s] IgM- cells) isolated from fetal bone marrow. Maximum growth inhibition of either leukemic or normal BCP was reached at low IL-4 concentrations (10 U/ml), and the effect was specifically neutralized by anti-IL-4 antibody. IL-4 was further found to induce the expression of CD20 antigen on BCP-ALL cells from a number of the cases examined (5 of 8), but in contrast to leukemic cells, IL-4 failed to induce CD20 antigen on normal BCP. Finally, IL-4 was found to induce neither the expression of cytoplasmic mu chain, nor the appearance of sIgM+ cells in cultures of normal or leukemic BCP. Our data indicate that IL-4 has the potential to inhibit cell proliferation in leukemic and normal human B lymphopoiesis but is unable to drive the transition from BCP to mature B cells.

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