Our results revealed that the RND-3 efflux pump is the most up-regulated among the RND pumps tested in clinical isolates. Flunarizine 2HCl Quantitative RT-PCR demonstrated that mutations in BCAL1672 result in the activation of the RND-3 efflux pump. Correlation of Bithionol antibiotic resistance and efflux pump activation revealed that all 14 B. cenocepacia isolates with efflux pump activity were resistant to chloramphenicol. Among them, 12 had mutations in the regulator gene BCAL1672. The RND-9 efflux operon belongs to the HAE-1 family, which includes proteins responsible for the extrusion of aminoglycosides, ethidium bromide, fluoroquinolones and b-lactams. In this study, three clinical isolates exhibited increased transcriptional expression of RND-9, whereas no mutations were found in the regulator BCAM1948 or the promoter region. Up-regulation of RND-9 efflux pump expression could be activated by an unknown transcriptional factor like the situation that the global activator MarA of E.coli that can increase the acrAB efflux pump expression. The efflux pump mechanisms for cefazidime resistance in B. cenocepacia isolates warrant further investigation. Among the 6 fluoroquinoloneresistant B. cepacia complex isolates, amino acid changes were found in the QRDR region of the gyrA gene, including Gly81Asp, Thr83Ile, and Asp87His. Recognition of tumor antigen by specific T cells is a necessary prerequisite for the induction of effective anti-tumor immune responses. This is initiated by cross-presentation, a phenomenon where professional antigen presenting cells such as dendritic cells capture, process, and present exogenous antigens through the class I pathway. Cross priming of na? ��ve CD8 T cells by professional APC invokes a program leading to tumor specific-cytotoxic T lymphocytes which proliferate and traffic to the tumor site where they ultimately attack and destroy tumor cells. The efficiency of cross-priming has been shown to be influenced by the level of APC activation and maturation status, as well as the properties of cross-presented antigen itself. Factors such as antigen dose, type, source, location of the antigenic determinant within the tumor protein, and subcellular location within tumor cells can affect crosspriming efficiency.