ABSTRACT
IL-16 is a ligand and chemotactic factor for CD4+ T cells. IL-16 inhibits the CD3 mediated lymphocyte activation and proliferation. The effects of IL-16 on the target cells are dependent on the cell type, the presence of co-activators etc. To understand the regulation function and mechanism of IL-16 on target cells, we used a 130 a.a. recombinant IL-16 to study its effects on the growth of Jurkat T leukemia cells in vitro. We found that the rIL-16 stimulated the proliferation of Jurkat cells at low dose (10−9M), but inhibited the growth of the cells at higher concentration (10−5M). Results showed that 10−5 M of rIL-16 treatment induced an enhanced apoptosis in Jurkat cells. The treatment blocked the expression of FasL, but up-regulated the c-myc and Bid expression in the cells. Pre-treatment of PKC inhibitor or MEK1 inhibitor markedly increased or decreased the rIL-16 induced growth-inhibiting effects on Jurkat cells, respectively. The results suggested that the rIL-16 might be a regulator for the growth or apoptosis of Jurkat cells at a dose-dependent manner. The growth-inhibiting effects of rIL-16 might be Fas/FasL independent, but, associated with the activation of PKC, up-regulated expression of c-Myc and Bid, and the participation of the ERK signal pathway in Jurkat cells.
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Acknowledgements
We thank Mrs. Wan Li JIANG for her assistance for Cell culture techniques. This work was supported by Major State Basic Research (973) Program of China (G1999053905).
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ZHANG, X., XU, Y. The associated regulators and signal pathway in rIL-16/CD4 mediated growth regulation in Jurkat cells. Cell Res 12, 363–372 (2002). https://doi.org/10.1038/sj.cr.7290138
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DOI: https://doi.org/10.1038/sj.cr.7290138


