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EFFECT OF INTERLEUKIN-10 ON NF-KB AND AP-1 ACTIVITIES IN INTERLEUKIN-2 DEPENDENT CD8 T-LYMPHOBLASTS
Tekijät: HURME M, HENTTINEN T, KARPPELIN M, VARKILA K, MATIKAINEN S
Kustantaja: ELSEVIER SCIENCE BV
Julkaisuvuosi: 1994
Lehti:: Immunology Letters
Tietokannassa oleva lehden nimi: IMMUNOLOGY LETTERS
Lehden akronyymi: IMMUNOL LETT
Vuosikerta: 42
Numero: 3
Aloitussivu: 129
Lopetussivu: 133
Sivujen määrä: 5
ISSN: 0165-2478
DOI: https://doi.org/10.1016/0165-2478(94)90075-2
Tiivistelmä
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.
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.
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