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Demonstration of functional CD40 in B-lineage acute lymphoblastic leukemia
cells in response to T-cell CD40 ligand
N Renard, M Lafage-Pochitaloff, I Durand, V Duvert, L Coignet, J Banchereau and S Saeland
Schering-Plough Laboratory for Immunological Research, Dardilly, France.
Because activated T cells were previously shown to induce proliferation of
human normal B-cell precursors (BCP) via the CD40 pathway, we investigated
the effects of T cells on leukemic blasts isolated from patients with
B-lineage acute lymphoblastic leukemia (BCP-ALL). An anti- CD3 activated
human CD4+ T-cell clone was found to induce significant call proliferation
in four of nine BCP-ALL samples analyzed. In one of these cases, the T-cell
effect was clearly dependent on interaction between CD40 and its ligand.
Accordingly, a more thorough analysis was performed on this particular
leukemia (case 461, adult early pre-B-ALL, mBCR+, Philadelphia+, i(9q)+).
Thus, autologous CD4+ T cells isolated from the patient were also able to
induce CD40-dependent proliferation of the leukemic blasts. Analysis of the
phenotype after coculture showed that, among the CD19+ cells, a proportion
gradually lost expression of CD10 and CD34, whereas some cells acquired
CD23. In addition, and in contrast with normal BCP, activated T cells
promoted maturation of a subset of the case 461 leukemic cells into surface
IgM+ cells. The leukemic origin of the cycling and the maturing cells was
assessed by the presence of i(9q), a chromosomal abnormality associated
with this leukemia and evidenced by fluorescence in situ hybridization.
Taken together, these results show that leukemic BCP can be activated via
CD40 but that not all cases display detectable stimulation in response to T
cells despite their expression of CD40. In addition, the present data
suggest that CD4+ T cells could potentially play a role in the physiology
of BCP-ALL.
Volume 87,
Issue 12,
pp. 5162-5170,
06/15/1996
Copyright © 1996 by The American Society of Hematology
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