{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T00:38:53Z","timestamp":1790901533958,"version":"4.1.0"},"reference-count":29,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,11,3]],"date-time":"2005-11-03T00:00:00Z","timestamp":1130976000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2006,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>B chronic lymphocytic leukemia (B\u2010CLL) cells express several members of the tumor necrosis factor (TNF) family, such as CD40L, CD30L, and TRAIL. By using the cDNA microarray technology, B\u2010CLL samples were found to overexpress receptor activator of nuclear factor kB (NF\u2010kB) ligand (RANKL), as compared to normal CD19<jats:sup>+<\/jats:sup> B cells. These findings were validated at the protein level by Western blot and flow cytometry analyses. Moreover, unlike primary normal B cells, leukemic B\u2010CLL cells showed surface expression of RANK, the cognate transmembrane receptor of RANKL. When added in vitro to B\u2010CLL cultures, either alone or in association with chlorambucil or fludarabine, recombinant RANKL did not significantly modulate cell viability, and it minimally affected the IL\u20108 expression\/release. On the other hand, treatment with RANK\u2010Fc chimera potently upregulated the release of IL\u20108 in the B\u2010CLL culture supernatants, suggesting involvement of reverse signaling through transmembrane RANKL in IL\u20108 induction. In turn, exposure of B\u2010CLL cells to recombinant IL\u20108 significantly decreased spontaneous apoptosis as well as chlorambucil\u2010 and fludarabine\u2010mediated cytoxicity in B\u2010CLL cells. Since IL\u20108 has been implicated in progression of B\u2010CLL disease, our findings suggest that, by upregulating IL\u20108, the RANKL\/RANK system may contribute to the pathogenesis of B\u2010CLL. J. Cell. Physiol. 207: 158\u2013164, 2006. \u00a9 2005 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.20547","type":"journal-article","created":{"date-parts":[[2005,11,16]],"date-time":"2005-11-16T14:49:29Z","timestamp":1132152569000},"page":"158-164","source":"Crossref","is-referenced-by-count":32,"title":["Role of the RANKL\/RANK system in the induction of interleukin\u20108 (IL\u20108) in B chronic lymphocytic leukemia (B\u2010CLL) 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