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

IL-16 is a ligand and chemotactic factor for CD4+ T cells. IL-16 inhibits the CD3 mediated lymphocyteactivation and proliferation. The effects of IL-16 on the target cells are dependent on the cell type, thepresence of co-activators etc. To understand the regulation function and mechanism of IL-16 on targetcells, we used a 130 a.a. recombinant IL-16 to study its effects on the growth of Jurkat T leukemia cellsin vitro. We found that the rIL-16 stimulated the proliferation of Jurkat cells at low dose (10-9M), butinhibited the growth of the cells at higher concentration (10-5M). Results showed that 10-5 M of rIL-16treatment induced an enhanced apoptosis in Jurkat cells. The treatment blocked the expression of FasL, butup-regulated the c-myc and Bid expression in the cells. Pre-treatment of PKC inhibitor or MEK1 inhibitormarkedly 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 ata 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 ofthe ERK signal pathway in Jurkat cells.