Effect of interleukin-10 on NF-kB and AP-1 activities in interleukin-2 dependent CD8 T lymphoblasts.
Interleukin-10 is a multifunctional cytokine, which regulates the function of various cell types of the immune system. In CD8 T cells it is known to accelerate the interleukin-2 dependent proliferation and to induce the differentiation of these cells to active cytolytic cells. Now we have studied interleukin-10 induced intracellular signaling mechanisms in human interleukin-2 dependent CD8 T lymphoblasts. The data obtained demonstrate that interleukin-10 alone can activate the AP-1 transcription factor and potentiate the interleukin-2 induced NF-kappa B activity. Moreover, interleukin-10 induced a rapid tyrosine phosphorylation of several proteins. The pattern of proteins phosphorylated was very similar to that induced by interleukin-2. Together, these findings suggest that tyrosine kinase dependent activation of NF-kappa B and AP-1 transcription factors are involved in the signaling mechanism of interleukin-10. This activation pathway resembles that of interleukin-2 in the same cell type.
Hurme
M
M
Department of Biomedical Sciences, University of Tampere, Finland.
Henttinen
T
T
Karppelin
M
M
Varkila
K
K
Matikainen
S
S
D001483:Base Sequence; D018414:CD8-Positive T-Lymphocytes / Q000187:drug effects* / Q000502:physiology; D002478:Cells, Cultured; D004591:Electrophoresis, Polyacrylamide Gel; D006801:Humans; D015151:Immunoblotting; D016753:Interleukin-10 / Q000494:pharmacology*; D007376:Interleukin-2 / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000276:immunology; D008969:Molecular Sequence Data; D016328:NF-kappa B / Q000502:physiology*; D010750:Phosphoproteins / Q000032:analysis; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000276:immunology; D018808:Transcription Factor AP-1 / Q000502:physiology*
D007376:Interleukin-2; D016328:NF-kappa B; D010750:Phosphoproteins; D018808:Transcription Factor AP-1; D016753:Interleukin-10; D011505:Protein-Tyrosine Kinases