the CD56 NK cell subset was a more mature cell population and displayed stable phenotype and function. On another hand, functionally related toCD8 Tcells,CD56 NKcells were strongly cytotoxic effector cells. Surprisingly, IL 15 protected chk inhibitor CD56 cells from apoptosis, as did on CD8 T cells. IL 15 better maintained the amount of CD56 NK cells from cord blood than from peripheral blood, even though we and others failed to make CD56 NK cells from cells. Besides that IL 15 maintained the proliferation and survival of CD56 NK cells, IL 15 might enhance CD56 NK cell differentiation from cord blood intermediateNKprecursors. The anti apoptotic Bcl 2 family proteins, Bcl 2 and Bcl xL, encourage cell survival by inhibition of mitochondria dependent extrinsic and intrinsic cell death pathways. IL 15 has been shown to be a strong apoptotic inhibitor in a number of forms of lymphocytes via induction of anti apoptotic molecules. It’s been proven that upregulation of Bcl 2 expression in activated Immune system T cells plays a key part in prevention of activated T cell apoptosis. But, our results indicated that IL15 induced substantial expression of Bcl xL, but not Bcl 2,was related to the inhibition of CD56 NK cells from apoptosis. Compared with CD56 NK cells, the expression of Bcl xL in CD56 NK cells made them vunerable to apoptosis. Bcl 2 and Bcl xL often played important role in anti apoptosis through function between these two proteins, as previously reported, however the crucial functions of each protein were somewhat different according to differential cell types or death signals. Therefore, why Bcl xL, although not Bcl 2, applied anti apoptotic impact of IL 15 on CD56 cells requires further confirmation. The difference in IL 2 or IL 15 pushed cell survival or apoptosis could be related to the various expressions of IL 2 and IL 15 receptor complexes. As critical signaling components the practical receptors for IL 2 and IL 15 include a private string, which defines the specificity for IL 2 and IL 15, and share IL 2R and stores. These receptor Icotinib subunits were expressed individually or in various combinations, leading to the formation of receptors with different affinities, unique signaling abilities or both. Generally, IL 2 bound like a soluble ligand to IL 2R, although IL 15 was regarded as trans presented by the IL 15R subunit to subunits on neighboring cells. So, the sign transduced by the IL 15R complex and that by the IL 2R complex may be qualitatively different, regardless of the sharing of signaling receptor elements and the normal. The expression of IL 2R on NK cells, especially CD56 cells, was up-regulated by IL 15 more highly than IL 2, and IL 15R expression on cord blood NK cells was better preserved by IL 15.

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