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TLR agonists work as adjuvants to modulate the function of mDCs. In TLR signaling, MyD88 and TRIF\/TICAM\u20101 are major TLR adaptor molecules, which when overexpressed are able to transduce downstream signals without TLR stimuli. We successfully introduced the adaptors into mouse bone marrowderived mDCs using lentiviral vectors. Introduction of MyD88 into mDCs in vitro led to the production of IL\u20106 and IL\u201012p40 while introduction of TICAM\u20101 stimulated interferon (IFN)\u2010alpha production. Expression of TICAM\u20101, but not MyD88, in mDCs slightly induced the co\u2010stimulatory molecule CD86, while significant upregulation of CD86 was observed in response to other TLR stimuli. Both MyD88 and TICAM\u20101 augmented allogeneic mixed lymphocyte reaction (MLR). Ex vivo mouse spleen cells pre\u2010exposed to tumor antigen exhibited antitumor cytotoxicity when incubated with MyD88\u2010 or TICAM\u20101\u2010expressing mDCs. Using mDC adoptive transfer and a syngeneic mouse tumor implant model, we established an antitumor immunotherapy whereby tumor growth is retarded by adaptor\u2010manipulated mDCs.<\/jats:p>","DOI":"10.1016\/j.febslet.2007.06.019","type":"journal-article","created":{"date-parts":[[2007,6,22]],"date-time":"2007-06-22T07:22:43Z","timestamp":1182496963000},"page":"3334-3340","source":"Crossref","is-referenced-by-count":22,"title":["Tumor immunotherapy using bone marrow\u2010derived dendritic cells overexpressing Toll\u2010like receptor 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