原创力文档rnai-mediated c-rel silencing leads to apoptosis of b cell tumor cells and suppresses antigenic immune response in vivornai-mediated沉默导致b细胞肿瘤细胞的凋亡和抑制体内抗原的免疫应答.pdfVIP
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rnai-mediated c-rel silencing leads to apoptosis of b cell tumor cells and suppresses antigenic immune response in vivornai-mediated沉默导致b细胞肿瘤细胞的凋亡和抑制体内抗原的免疫应答
RNAi-Mediated c-Rel Silencing Leads to Apoptosis of B
Cell Tumor Cells and Suppresses Antigenic Immune
Response In Vivo
Wenzhi Tian, Hsiou-Chi Liou*
Division of Immunology, Department of Medicine, Weill Medical College of Cornell University, New York, New York, United States of America
Abstract
c-Rel is a member of the Rel/NF-kB transcription factor family and is predominantly expressed in lymphoid and myeloid
cells, playing a critical role in lymphocyte proliferation and survival. Persistent activation of the c-Rel signal transduction
pathway is associated with allergies, inflammation, autoimmune diseases, and a variety of human malignancies. To explore
the potential of targeting c-Rel as a therapeutic agent for these disorders, we designed a small interfering RNA (siRNA) to
silence c-Rel expression in vitro and in vivo. C-Rel-siRNA expression via a retroviral vector in a B cell tumor cell line leads to
growth arrest and apoptosis of the tumor cells. Silencing c-Rel in primary B cells in vitro compromises their proliferative and
survival response to CD40 activation signals, similar to the impaired response of c-Rel knockout B cells. Most important, in
vivo silencing of c-Rel results in significant impairment in T cell-mediated immune responses to antigenic stimulation. Our
study thus validates the efficacy of c-Rel-siRNA, and suggests the development of siRNA-based therapy, as well as small
molecular inhibitors for the treatment of B cell tumors as well as autoimmune diseases.
Citation: Tian W, Liou H-C (2009) RNAi-Mediated c-Rel Silencing Leads to Apoptosis of B Cell Tumor Cells and Suppresses Antigenic Immune Response In
Vivo. PLoS ONE 4(4): e5028. doi:10.1371/journal.pone.0005028
Editor: Mikhail V. Blagosklonny, Ordway Research Institute, United States of America
Received December 19, 2008; Accepted March 5, 2009; Published April 6, 2009
Copyright: 20
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