Designing and establishment of ISO/IEC 17025 in laboratories of national inland water aquaculture center and south Iran aquaculture research center

The project was carried out between June of 2011 and November of 2012,8 laboratories of research center in Anzali (Plankton, Algae, Hydrochemistry, Physiology, Ichthyology, Bentose, Parazitology, Virology) and 7 laboratories of research center in Ahvaz (Clinical pathology, Plankton, Hydrochemistry, Physiology, Ichthyology, Bentose, Parazitology, Virology) were selected for accreditation. The main stages for establishment of the system consisted of: 1-Conducting a gap analysis to compare the present state of the laboratories with ISO/IEC 17025 2-Training General requirements for the competence of testing and calibration laboratories Validation of methods Estimation of uncertainty Internal audits 3- Performing of technical and management requirements 4-Submit of quality manual to ASCB center in England in order to accredit In August of 2012 The main results were including: 1-Increase the accuracy of measurement in laboratories 2-Improvement of the Repeatability and Reproducibility of the test methods 3-Traceability and standardization of test methods 4- Calibration of measurement instruments 6- Updating of test methods 7-Standardization of physical condition of the laboratories 8- Getting the certification from ASCB center i

TGF-β and CIS inhibition overcomes NK cell suppression to restore anti-tumor immunity

Antibodies targeting “immune checkpoints” have revolutionized cancer therapy by reactivating tumor-resident cytotoxic lymphocytes, primarily CD8þ T cells. Interest in targeting analogous pathways in other cytotoxic lymphocytes is growing. Natural killer (NK) cells are key to cancer immunosurveillance by eradicating metastases and driving solid tumor inflammation. NK-cell antitumor function is dependent on the cytokine IL15. Ablation of the IL15 signaling inhibitor CIS (Cish) enhances NK-cell antitumor immunity by increasing NK-cell metabolism and persistence within the tumor microenvironment (TME). The TME has also been shown to impair NK-cell fitness via the production of immuno-suppressive transforming growth factor b (TGFb), a suppression which occurs even in the presence of high IL15 signaling. Here, we identified an unexpected interaction between CIS and the TGFb signaling pathway in NK cells. Independently, Cish- and Tgfbr2- deficient NK cells are both hyperresponsive to IL15 and hyporesponsive to TGFb, with dramatically enhanced antitumor immunity. Remarkably, when both these immunosuppressive genes are simultaneously deleted in NK cells, mice are largely resistant to tumor development, suggesting that combining suppression of these two pathways might represent a novel therapeutic strategy to enhance innate anticancer immunity.Fernando Souza-Fonseca-Guimaraes, Gustavo R. Rossi, Laura F. Dagley, Momeneh Foroutan, Timothy R. McCulloch, Jumana Yousef, Hae-Young Park, Jennifer H. Gunter, Paul A. Beavis, Cheng-Yu Lin, Soroor Hediyeh-Zadeh, Tania Camilleri, Melissa J. Davis, and Nicholas D. Huntingto

TGFβ and CIS Inhibition Overcomes NK-cell Suppression to Restore Antitumor Immunity

Antibodies targeting “immune checkpoints” have revolutionized cancer therapy by reactivating tumor-resident cytotoxic lymphocytes, primarily CD8+ T cells. Interest in targeting analogous pathways in other cytotoxic lymphocytes is growing. Natural killer (NK) cells are key to cancer immunosurveillance by eradicating metastases and driving solid tumor inflammation. NK-cell antitumor function is dependent on the cytokine IL15. Ablation of the IL15 signaling inhibitor CIS (Cish) enhances NK-cell antitumor immunity by increasing NK-cell metabolism and persistence within the tumor microenvironment (TME). The TME has also been shown to impair NK-cell fitness via the production of immunosuppressive transforming growth factor β (TGFβ), a suppression which occurs even in the presence of high IL15 signaling. Here, we identified an unexpected interaction between CIS and the TGFβ signaling pathway in NK cells. Independently, Cish- and Tgfbr2-deficient NK cells are both hyperresponsive to IL15 and hyporesponsive to TGFβ, with dramatically enhanced antitumor immunity. Remarkably, when both these immunosuppressive genes are simultaneously deleted in NK cells, mice are largely resistant to tumor development, suggesting that combining suppression of these two pathways might represent a novel therapeutic strategy to enhance innate anticancer immunity.</p