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 Blood, 1 August 2005, Vol. 106, No. 3, pp. 1012-1020.
Prepublished online as a Blood First Edition Paper on April 28, 2005; DOI 10.1182/blood-2004-03-0889.

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NEOPLASIA

Nurselike cells express BAFF and APRIL, which can promote survival of chronic lymphocytic leukemia cells via a paracrine pathway distinct from that of SDF-1{alpha}

Mitsufumi Nishio, Tomoyuki Endo, Nobuhiro Tsukada, Junko Ohata, Shinichi Kitada, John C. Reed, Nathan J. Zvaifler, and Thomas J. Kipps

From the Department of Medicine, University of California, San Diego, La Jolla; and The Burnham Institute, La Jolla, CA.

We examined expression of B cell–activating factor of the tumor necrosis factor (TNF) family (BAFF) and a proliferation-inducing ligand (APRIL) on chronic lymphocytic leukemia (CLL) B cells and nurselike cells (NLCs), which differentiate from CD14+ cells when cultured with CLL B cells. NLCs expressed significantly higher levels of APRIL than monocytes and significantly higher levels of BAFF and APRIL than CLL B cells. Also, the viability of CLL B cells cultured with NLCs was significantly reduced when CLL B cells were cultured with decoy receptor of B-cell maturation antigen (BCMA), which can bind both BAFF and APRIL, but not with BAFF receptor:Fc (BAFF-R:Fc), which binds only to BAFF. The effect(s) of BAFF or APRIL on leukemia cell survival appeared additive and distinct from that of stromal cell–derived factor-1{alpha} (SDF-1{alpha}), which in contrast to BAFF or APRIL induced leukemia cell phosphorylation of p44/42 mitogen-activated protein kinase (extracellular signal-regulated kinase-1/2 [ERK1/2]) and AKT. Conversely, BAFF and APRIL, but not SDF-1{alpha}, induced CLL-cell activation of the nuclear factor–{kappa}B1 (NF-{kappa}B1) and enhanced CLL-cell expression of the antiapoptotic protein Mcl-1. However, BAFF, but not APRIL, also induced CLL-cell activation of NF-{kappa}B2. We conclude that BAFF and APRIL from NLCs can function in a paracrine manner to support leukemia cell survival via mechanisms that are distinct from those of SDF-1{alpha}, indicating that NLCs use multiple distinct pathways to support CLL-cell survival.


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