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Blood, 15 January 2004, Vol. 103, No. 2, pp. 679-688.
Prepublished online as a Blood First Edition Paper on September 22, 2003; DOI 10.1182/blood-2003-02-0540.
 Previous Article | Table of Contents | Next Article 
NEOPLASIA
Involvement of BAFF and APRIL in the resistance to apoptosis of B-CLL through an autocrine pathway
Catherine Kern,
Jean-François Cornuel,
Christian Billard,
Ruoping Tang,
Danielle Rouillard,
Virginie Stenou,
Thierry Defrance,
Florence Ajchenbaum-Cymbalista,
Pierre-Yves Simonin,
Sophie Feldblum, and
Jean-Pierre Kolb
From the U365 Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Curie, Paris, France; Neurolab, Paris, France; EA1529/EMI9912, Service d'Hématologie, Paris, France; Service de Cytométrie, Institut Curie, Paris, France; and U404 INSERM, Lyon, France.
Tumor necrosis factor (TNF) superfamily members BAFF, or B-cell activation factor of the TNF family, and APRIL, a proliferation-inducing ligand, are involved in normal B-cell survival and differentiation. They interact with 3 receptors: BAFF-R, specific to BAFF; and TACI and BCMA, which are shared by BAFF and APRIL. We tested the potential role of these proteins in B-cell chronic lymphocytic leukemia (B-CLL) resistance to apoptosis. TACI and BAFF-R mRNAs were found in leukemic B cells. BAFF and APRIL mRNAs and proteins were detected in B-CLL leukemic cells and normal blood or tonsil-derived B lymphocytes. Yet, in contrast to normal B lymphocytes, BAFF and APRIL were expressed at the membranes of leukemic cells. Adding soluble BAFF or APRIL protected B-CLL cells against spontaneous and drug-induced apoptosis and stimulated NF- B activation. Conversely, adding soluble BCMA-Fc or anti-BAFF and anti-APRIL antibodies enhanced B-CLL apoptosis. Moreover, a soluble form of BAFF was detected using surface-enhanced laser desorption/ionization–time-of-flight mass spectrometry (SELDI-TOF MS) in the sera of B-CLL patients but not of healthy donors. Taken together, our results indicate that B-CLL cells can be rescued from apoptosis through an autocrine process involving BAFF, APRIL, and their receptors. Inhibiting BAFF and APRIL pathways may be of therapeutic value for B-CLL treatment.
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