SEARCH:   Advanced

Blood, 15 January 2007, Vol. 109, No. 2, pp. 729-739. Prepublished online as a Blood First Edition Paper on September 7, 2006; DOI 10.1182/blood-2006-04-015958. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-04-015958v1 109/2/729    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Chiu, A. Articles by Cerutti, A. Search for Related Content PubMed PubMed Citation Articles by Chiu, A. Articles by Cerutti, A. Related Collections Neoplasia Apoptosis Cell Cycle Signal Transduction Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Hodgkin lymphoma cells express TACI and BCMA receptors and generate survival and proliferation signals in response to BAFF and APRIL April Chiu1, Weifeng Xu1, Bing He1, Stacey R. Dillon2, Jane A. Gross2, Eric Sievers2, Xugang Qiao1, Paul Santini1, Elizabeth Hyjek1, Joong-won Lee1, Ethel Cesarman1,3, Amy Chadburn1, Daniel M. Knowles1, and Andrea Cerutti1,3, 1 Department of Pathology and Laboratory Medicine of Weill Medical College of Cornell University, New York, NY; 2 ZymoGenetics, Seattle, WA; 3 Graduate Program of Immunology and Microbial Pathogenesis, Weill Graduate School of Medical Sciences of Cornell University, New York, NY Hodgkin lymphoma (HL) originates from the clonal expansion of malignant Hodgkin and Reed-Sternberg (HRS) cells. These B-cell–derived elements constitute less than 10% of the tumoral mass. The remaining tissue is comprised of an inflammatory infiltrate that includes myeloid cells. Myeloid cells activate B cells by producing BAFF and APRIL, which engage TACI, BCMA, and BAFF-R receptors on the B cells. Here, we studied the role of BAFF and APRIL in HL. Inflammatory and HRS cells from HL tumors expressed BAFF and APRIL. Unlike their putative germinal center B-cell precursors, HRS cells lacked BAFF-R, but expressed TACI and BCMA, a phenotype similar to that of plasmacytoid B cells. BAFF and APRIL enhanced HRS cell survival and proliferation by delivering nonredundant signals via TACI and BCMA receptors through both autocrine and paracrine pathways. These signals caused NF-B activation; Bcl-2, Bcl-xL, and c-Myc up-regulation; and Bax down-regulation, and were amplified by APRIL-binding proteoglycans on HRS cells. Interruption of BAFF and APRIL signaling by TACI-Ig decoy receptor, which binds to and neutralizes BAFF and APRIL, or by small-interfering RNAs targeting BAFF, APRIL, TACI, and BCMA inhibited HRS cell accumulation in vitro and might attenuate HL expansion in vivo. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. Brady, H. J. Whiteman, L. C. Spender, and P. J. Farrell Downregulation of RUNX1 by RUNX3 Requires the RUNX3 VWRPY Sequence and Is Essential for Epstein-Barr Virus-Driven B-Cell Proliferation J. Virol., July 1, 2009; 83(13): 6909 - 6916. [Abstract] [Full Text] [PDF] V. F.-S. Shih, J. D. Kearns, S. Basak, O. V. Savinova, G. Ghosh, and A. Hoffmann Kinetic control of negative feedback regulators of NF-{kappa}B/RelA determines their pathogen- and cytokine-receptor signaling specificity PNAS, June 16, 2009; 106(24): 9619 - 9624. [Abstract] [Full Text] [PDF] M. Gupta, S. R. Dillon, S. C. Ziesmer, A. L. Feldman, T. E. Witzig, S. M. Ansell, J. R. Cerhan, and A. J. Novak A proliferation-inducing ligand mediates follicular lymphoma B-cell proliferation and cyclin D1 expression through phosphatidylinositol 3-kinase-regulated mammalian target of rapamycin activation Blood, May 21, 2009; 113(21): 5206 - 5216. [Abstract] [Full Text] [PDF] A. J. Novak, S. L. Slager, Z. S. Fredericksen, A. H. Wang, M. M. Manske, S. Ziesmer, M. Liebow, W. R. Macon, S. R. Dillon, T. E. Witzig, et al. Genetic Variation in B-Cell-Activating Factor Is Associated with an Increased Risk of Developing B-Cell Non-Hodgkin Lymphoma Cancer Res., May 15, 2009; 69(10): 4217 - 4224. [Abstract] [Full Text] [PDF] F. C. Kimberley, L. van Bostelen, K. Cameron, G. Hardenberg, J. A. Marquart, M. Hahne, and J. P. Medema The proteoglycan (heparan sulfate proteoglycan) binding domain of APRIL serves as a platform for ligand multimerization and cross-linking FASEB J, May 1, 2009; 23(5): 1584 - 1595. [Abstract] [Full Text] [PDF] D. Bonci, M. Musumeci, V. Coppola, A. Addario, C. Conticello, M. Hahne, M. Gulisano, F. Grignani, and R. De Maria Blocking the APRIL circuit enhances acute myeloid leukemia cell chemosensitivity Haematologica, December 1, 2008; 93(12): 1899 - 1902. [Abstract] [Full Text] [PDF] W. Xu, P. A. Santini, A. J. Matthews, A. Chiu, A. Plebani, B. He, K. Chen, and A. Cerutti Viral Double-Stranded RNA Triggers Ig Class Switching by Activating Upper Respiratory Mucosa B Cells through an Innate TLR3 Pathway Involving BAFF J. Immunol., July 1, 2008; 181(1): 276 - 287. [Abstract] [Full Text] [PDF] S. K. Chang, S. A. Mihalcik, and D. F. Jelinek B Lymphocyte Stimulator Regulates Adaptive Immune Responses by Directly Promoting Dendritic Cell Maturation J. Immunol., June 1, 2008; 180(11): 7394 - 7403. [Abstract] [Full Text] [PDF] V. T. Chu, P. Enghard, G. Riemekasten, and C. Berek In Vitro and In Vivo Activation Induces BAFF and APRIL Expression in B Cells J. Immunol., November 1, 2007; 179(9): 5947 - 5957. [Abstract] [Full Text] [PDF] M. C. Ryan, M. Hering, D. Peckham, C. F. McDonagh, L. Brown, K. M. Kim, D. L. Meyer, R. F. Zabinski, I. S. Grewal, and P. J. Carter Antibody targeting of B-cell maturation antigen on malignant plasma cells Mol. Cancer Ther., November 1, 2007; 6(11): 3009 - 3018. [Abstract] [Full Text] [PDF]

	Copyright © 2007 by American Society of Hematology         Online ISSN: 1528-0020