Chronic lymphocytic leukemia disease progression is accelerated by APRIL-TACI interaction in the TCL1 transgenic mouse model

Valeria Lascano, Marco Guadagnoli, Jan G. Schot, Dieuwertje M. Luijks, Jeroen E. J. Guikema, Katherine Cameron, Michael Hahne, Steven Pals, Erik Slinger, Thomas J. Kipps, Marinus H. J. van Oers, Eric Eldering, Jan Paul Medema, Arnon P. Kater

Research output: Contribution to journalArticleAcademicpeer-review

20 Citations (Scopus)


Although in vitro studies pointed to the tumor necrosis factor family member APRIL (a proliferation-inducing ligand) in mediating survival of chronic lymphocytic leukemia (CLL) cells, clear evidence for a role in leukemogenesis and progression in CLL is lacking. APRIL significantly prolonged in vitro survival of CD5(+)B220(dull) leukemic cells derived from the murine E mu-TCL1-Tg (TCL1-Tg [transgenic]) model for CLL. APRIL-TCL1 double-Tg mice showed a significantly earlier onset of leukemia and disruption of splenic architecture, and survival was significantly reduced. Interestingly, clonal evolution of CD5(+) B220(dull) cells (judged by BCR clonality) did not seem to be accelerated by APRIL; both mouse strains were oligoclonal at 4 months. Although APRIL binds different receptors, APRIL-mediated leukemic cell survival depended on tumor necrosis factor receptor superfamily member 13B (TACI) ligation. These findings indicate that APRIL has an important role in CLL and that the APRIL-TACI interaction might be a selective novel therapeutic target for human CLL. (Blood. 2013;122(24):3960-3963)
Original languageEnglish
Pages (from-to)3960-3963
Issue number24
Publication statusPublished - 2013

Cite this