Abstract.It has been previously demonstrated that cytokine-induced killer (CIK) cells possess potent cytotoxicity against various cancer cells, including lung cancer cells. However, the mechanism by which CIK cells recognize lung cancer cells has not been understood. The interaction between killer cell lectin like receptor K1 (NKG2D) receptor and NKG2D ligands was demonstrated to serve an important role in target cell killing by natural killer cells. The present study investigated whether NKG2D receptor and NKG2D ligand interactions are involved in the CIK-directed killing of lung cancer cells. The expression of MICA and ULBP2 was detected in tumor and healthy tissue samples. The expression of MICA and ULBP2 in tumor tissue samples was higher compared with that in the healthy control tissue. The expression of NKG2D ligands was analyzed in A549 and Q56 cells through reverse transcription-quantitative polymerase chain reaction and flow cytometry. The results demonstrated that the lung cancer cell lines markedly expressed the NKG2D ligands. Furthermore, NKG2D ligand-expressing lung cancer cells were targeted by CIK cells, which was partially blocked by treating CIK cells with an antibody against NKG2D. The data of the current study has demonstrated that the NKG2D-NKG2D ligand interaction serves an essential role in mediating lung cancer cell killing by CIK cells.
The Curie temperature of diluted magnetic semiconductor (DMS) nanowires and nanoslabs is investigated using the mean-field model. The Curie temperature in DMS nanowires can be much larger than that in corresponding bulk material due to the density of states of one-dimensional quantum wires, and when only one conduction subband is filled, the Curie temperature is inversely proportional to the carrier density. The TC in DMS nanoslabs is dependent on the carrier density through the number of the occupied subbands. A transverse electric field can change the DMS nanowires from the paramagnet to ferromagnet, or vice versae.
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