Role of JAK2 signal transductional pathway in activation and survival of human peripheral eosinophils by interferon-gamma (IFN-γ)
| Autor: | Takao Sugiyama, E Tanabe, M Sueishi, M Kagami, Kenichi Ochiai, C. Ishihara, Koya N, Hisao Tomioka |
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| Rok vydání: | 1999 |
| Předmět: |
Adult
Antigens Differentiation T-Lymphocyte Male Adolescent Cell Survival medicine.medical_treatment Immunology Biology Lymphocyte Activation Interferon-gamma chemistry.chemical_compound Western blot Antigens CD Proto-Oncogene Proteins Eosinophil activation medicine Humans Immunology and Allergy Lectins C-Type Interferon gamma Enzyme Inhibitors Phosphorylation Cells Cultured Eosinophil cationic protein Dose-Response Relationship Drug medicine.diagnostic_test Tyrosine phosphorylation Original Articles Janus Kinase 2 Middle Aged Protein-Tyrosine Kinases Tyrphostins respiratory system Eosinophil Eosinophils medicine.anatomical_structure Cytokine chemistry Cancer research Female Signal transduction Signal Transduction medicine.drug |
| Zdroj: | Clinical and Experimental Immunology. 118:340-343 |
| ISSN: | 1365-2249 0009-9104 |
| DOI: | 10.1046/j.1365-2249.1999.01068.x |
| Popis: | SUMMARYThe purpose of this study was to determine whether the JAK pathway is involved in eosinophil activation and survival through IFN-γ receptor signalling in human peripheral eosinophils. Eosinophils were purified from the blood of six atopic disease patients by anti-CD16 magnetic bead-negative selection. IFN-γ significantly up-regulated survival and CD69 expression in 24–48 h cultured eosinophils. Further, IFN-γ induced tyrosine phosphorylation of JAK2 in eosinophils, as indicated by Western blot analysis. Finally, the specific JAK2 inhibitor AG-490 inhibited the tyrosine phosphorylation of JAK2, IFN-γ-induced survival and CD69 expression in eosinophils. In conclusion, these results indicate that IFN-γ induces eosinophil survival and CD69 expression through the activation of JAK2 in peripheral eosinophils, suggesting that JAK2 may play a significant role in eosinophil regulation by IFN-γ–IFN-γR interaction. |
| Databáze: | OpenAIRE |
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