PMID- 20217563 OWN - NLM STAT- MEDLINE DCOM- 20100517 LR - 20100310 IS - 1940-6029 (Electronic) IS - 1064-3745 (Linking) VI - 623 DP - 2010 TI - Preventing immune rejection through gene silencing. PG - 357-71 LID - 10.1007/978-1-60761-588-0_23 [doi] AB - Dendritic cells (DCs) comprise a family of professional antigen-presenting cells responsible for the induction of primary immune responses. DCs are also important for the induction of immunological tolerance. Recent research has revealed that DC maturation is associated with activation of the NF-kappaB pathway. RelB, one of the five families of Rel proteins involved in the NF-kappaB pathway, plays a critical role in coordinating the terminal stages of DC maturation and has the ability to induce optimal Th1 T cell responses. DCs generated from mouse bone marrow can be silenced using siRNA specific for the target gene. Silencing RelB in DCs will result in the generation of immunoregulatory dendritic cells that inhibit allogenic T cell responses. The KLH-specific T cell response should also be inhibited after the RelB siRNA treatment. Furthermore, silencing the RelB gene in DCs can generate regulatory T cells. Administering donor-derived RelB-silencing DCs can prevent allograft rejection in murine heart transplantation. FAU - Zhang, Xusheng AU - Zhang X AD - Department of Surgery, University of Western Ontario, London, ON, Canada. FAU - Li, Mu AU - Li M FAU - Min, Wei-Ping AU - Min WP LA - eng PT - Journal Article PL - United States TA - Methods Mol Biol JT - Methods in molecular biology (Clifton, N.J.) JID - 9214969 RN - 0 (Relb protein, mouse) RN - 147337-75-5 (Transcription Factor RelB) SB - IM MH - Animals MH - Bone Marrow Cells/immunology MH - Dendritic Cells/*immunology/metabolism MH - Flow Cytometry MH - *Gene Silencing MH - Heart Transplantation/*immunology MH - *Immune Tolerance MH - Male MH - Mice MH - Mice, Inbred C57BL MH - T-Lymphocytes, Regulatory/immunology MH - Tissue Donors MH - Transcription Factor RelB/genetics EDAT- 2010/03/11 06:00 MHDA- 2010/05/18 06:00 CRDT- 2010/03/11 06:00 PHST- 2010/03/11 06:00 [entrez] PHST- 2010/03/11 06:00 [pubmed] PHST- 2010/05/18 06:00 [medline] AID - 10.1007/978-1-60761-588-0_23 [doi] PST - ppublish SO - Methods Mol Biol. 2010;623:357-71. doi: 10.1007/978-1-60761-588-0_23.