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학술저널

노령의 랫드에서 분리한 자연살해 세포의 활성 강화 효과 및 활성 강화된 자연살해 세포의 IL-2 분비능 조사

Study on the characterization of augmented natural killer cells isolated from peripheral blood lymphocytes in old rat

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Natural killer cells have now become established as a unique lymphocyte subset associated with a wide array of important biological functions. This study was performed to examine the characteristics of the large granular lymphocyte(LGL, natural killer cell; NK cell) which was augmented by cytokines and mitogens, and the secretion of the interleukin-2(IL-2) from the augmented LGL. The total T lymphocytes and the LGL were purified from peripheral blood lymphocytes of Sprague-Dawley male rat from 16 to 30 weeks old. Peripheral blood was collected by cardiac puncture. As augmenting agents, IL-2, granulocyte-macrophage colony stimulating factor(GM-CSF), polyinosinic-polycytidylic acid(Poly I:C) and lectin were used. After treatment of these agents to total T lymphocytes and LGL at various concentration, we examined the proliferation of T lymphocytes and LGL, the conjugation activity of LGL for the YAC-1 and the autogenous IL-2 secretion from LGL. As results, the proliferation was significantly increased in total T lymphocytes which were treated with poly I:C(p<0.05) and lectin(p<0.05) at 12.5㎍/ml and 25㎍/ml concentration, respectively. However, the proliferation of LGL was not observed in any treatments. The conjugation activity was significantly increased(p<0.05) in LGL treated with IL-2 of 15 U/ml and poly I:C of 25㎍/ml for 3 hours. In addition, the activity of LGL treated with poly I:C of 25㎍/ ml for 6 hours was also significantly augmented(p<0.05). Autogenous IL-2 secretion evaluated by the CTLL-2 proliferation assay was confirmed in groups treated with IL-2 and poly I:C, and the proliferation by poly I:C was more effective than that of IL-2. These results suggest that the functional activity of LGL on the conjugation activity and the autogenous IL-2 secretion were increased by Poly I:C, but the proliferation of LGL was not observed.

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