title: The associated regulators and signal pathway in rIL-16/CD4 mediated growth regulation in Jurkat cells.
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(-9)M), but inhibited the growth of the cells at higher concentration (10(-5)M). 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.
authors.affiliation: Lab of Molecular and Cellular Oncology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China.
authors.forename: Xiao Ming
authors.initials: XM
authors.lastname: Zhang
authors.forename: Yong Hua
authors.initials: YH
authors.lastname: Xu
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D051023:BH3 Interacting Domain Death Agonist Protein; D015704:CD4 Antigens / Q000276:immunology* / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D002352:Carrier Proteins / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D018797:Cell Cycle Proteins / Q000235:genetics / Q000276:immunology; D002455:Cell Division / Q000187:drug effects / Q000235:genetics / Q000276:immunology*; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D053222:Fas Ligand Protein; D006801:Humans; D019410:Interleukin-16 / Q000235:genetics / Q000276:immunology* / Q000494:pharmacology; D019169:Jurkat Cells; D015458:Leukemia, T-Cell / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D008562:Membrane Glycoproteins / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D011493:Protein Kinase C / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D016271:Proto-Oncogene Proteins c-myc / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D011993:Recombinant Fusion Proteins / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics / Q000276:immunology*
chemical_list: D051023:BH3 Interacting Domain Death Agonist Protein; C494814:BID protein, human; D015704:CD4 Antigens; D002352:Carrier Proteins; D018797:Cell Cycle Proteins; D004791:Enzyme Inhibitors; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D019410:Interleukin-16; D008562:Membrane Glycoproteins; D016271:Proto-Oncogene Proteins c-myc; D011993:Recombinant Fusion Proteins; D011493:Protein Kinase C