REGULAR ARTICLES

Cell Research (2002); 12(5-6):363-372

The associated regulators and signal pathway in rIL-16/CD4 mediated growth regulation in Jurkat cells

Xiao Ming ZHANG, Yong Hua XU^*

Lab of Molecular and Cellular Oncology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China

Received Jul-5-2002  Revised Oct-25-2002 Accepted Nov-7-2002

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.

Key words: IL-16, Jurkat cells, growth regulation.