Differential Effects of Tyrosine Kinase Inhibition in CD69 Antigen Expression and Lytic Activity Induced by rIL-2, rIL-12, and rIFN-α in Human NK Cells
Autor: | Claudia Benati, Giuseppe Carra, Franca Gerosa, Giorgio Trinchieri, Giorgio Gandini, Marina Tommasi, Massimo Libonati, Giuseppe Tridente |
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Rok vydání: | 1993 |
Předmět: |
Antigens
Differentiation T-Lymphocyte Cytotoxicity Immunologic Interleukin 2 medicine.medical_treatment Immunology chemical and pharmacologic phenomena Biology Natural killer cell Antigen Antigens CD parasitic diseases medicine Humans Lectins C-Type Cells Cultured Interferon alfa Interleukins Interferon-alpha hemic and immune systems Protein-Tyrosine Kinases Genistein Interleukin-12 Isoflavones Molecular biology Recombinant Proteins biological factors Killer Cells Natural medicine.anatomical_structure Cytokine Cell culture Cancer research Interleukin 12 Interleukin-2 Tyrosine kinase medicine.drug |
Zdroj: | Cellular Immunology. 150:382-390 |
ISSN: | 0008-8749 |
DOI: | 10.1006/cimm.1993.1206 |
Popis: | The effect of rIL-12 on induction of CD69 antigen expression and cytolytic activity in purified human NK cells was evaluated in comparison to the effects of rIL-2 and rIFN-alpha. It was found that rIL-12 directly induced CD69 antigen expression in NK cells, although the period of incubation required by rIL-12 was longer than the period required by rIL-2 or by rIFN-alpha. Similarly, the cytolytic activity induced by rIL-12 in NK cells against the NK-resistant target cell line Raji was consistently lower than the cytolytic activity induced by rIL-2 or rIFN-alpha when measured after 6 hr of incubation, and increased during the following 18 hr of incubation. To compare the involvement of tyrosin kinases in activation of NK cells induced by rIL-2, rIL-12, and rIFN-alpha, the effect of the specific inhibitor of tyrosin kinases, genistein, was evaluated on induction of CD69 antigen expression and lytic function mediated by the three cytokines. It was found that genistein inhibited CD69 antigen expression induced by rIL-2 and by rIL-12, but not that induced by rIFN-alpha. Unlike the effect on CD69 antigen expression, the cytolytic activity induced by all three cytokines was inhibited by genistein. These results, together with the finding that CD69 antigen expression induced by rIL-2 but not by rIL-12 or rIFN-alpha was inhibited by addition of rIL-4, strongly suggest that IL-2, IL-12, and IFN-alpha mediate their effects, leading to induction of CD69 antigen expression through different activation pathways. |
Databáze: | OpenAIRE |
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