MICB Human ELISA Kit

Natural cytotoxicity receptors and NKG2D correspond to major activating receptors involved in triggering of tumor cell lysis by human NK cells. In this report, we investigated the expression of NKG2D ligands (NKG2DLs), MHC class I-related chain (MIC) A, MICB and UL16-binding proteins 1, 2 and 3, on a panel of human non-small-cell lung carcinoma cell lines, and we analyzed their role in tumor cell susceptibility to NK cell lysis. Although adenocarcinoma (ADC) cells expressed heterogeneous levels of NKG2DLs, they were often resistant to NK cell-mediated killing. Resistance of a selected cell line, ADC-Coco, to allogeneic polyclonal NK cells and autologous NK cell clones correlated with shedding of NKG2DLs resulting from a matrix metalloproteinase (MMP) production. Treatment of ADC-Coco cells with a MMP inhibitor (MMPI) combined with IL-15 stimulation of autologous NK cell clones lead to a potentiation of NK cell-mediated cytotoxicity. This lysis is mainly NKG2D mediated, since it is abrogated by anti-NKG2D-neutralizing mAb. These results suggest that MMPIs, in combination with IL-15, may be useful for overcoming tumor cell escape from the innate immune response.

Major histocompatibility complex class I-related chain A and B (MICA/B) function in the regulation of protective responses due to stress induced expression. One of the major causes of the morbidity is sepsis. The objective of this study was to measure the mRNA levels of these genes in the control and sepsis patient groups. Data showed increases in mRNA concentrations of MICA and MICB in the Patient Group in contrast to the Control Group. However this level was found higher than MICA mRNA concentration in the patient group. The current study is the first report according to the researchers' knowledge representing the significant increases in the MICA and MICB expressions in the sepsis. This might provide a useful data for emphasizing these molecules as sensitive biomarkers. Further research is needed to enlighten the detail mechanisms of the MICA/B roles and to develop new treatment approaches.