Expression of Th17-related genes in PHA/IL-2-activated human T cells by Fas signaling via caspase-1- and Stat3-dependent pathway
| Autor: | Bei Chang Yang, Yu Ping Lin, Chung Chen Su, Yan Shen Shan, Huan Ching Lin |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
STAT3 Transcription Factor
Fas Ligand Protein T-Lymphocytes Immunology Blotting Western Caspase 1 Gene Expression Biology Lymphocyte Activation Stat3 Signaling Pathway Fas ligand Jurkat Cells RAR-related orphan receptor gamma Cell Line Tumor Cytotoxic T cell Humans fas Receptor Phosphorylation Phytohemagglutinins Cells Cultured Mitogen-Activated Protein Kinase 1 Caspase 8 Mitogen-Activated Protein Kinase 3 Reverse Transcriptase Polymerase Chain Reaction Interleukin-17 Models Immunological Nuclear Receptor Subfamily 1 Group F Member 3 Fas receptor Cell biology Interleukin-2 Th17 Cells Interleukin 17 Signal transduction Signal Transduction |
| Zdroj: | Cellular immunology. 281(2) |
| ISSN: | 1090-2163 |
| Popis: | T helper 17 (Th17) cells, which produce interleukin 17 (IL-17), are involved in the pathogenesis of autoimmune diseases and inflammatory conditions. Th17 cells have been detected in many Fas ligand-positive tumors. This study investigates the expression of Th17-related genes in PHA/IL-2-activated human T cells upon Fas ligation. Activated T cells transiently express RORγt, IL-17A, and IL-17F. A subsequent Fas receptor stimulation or contact with FasL-expressing glioma cells significantly prolongs the induction of RORγt and Th17-related cytokines. Treatments with inhibitors of caspase-1 and Stat3 reduce the Fas-signal-associated induction of RORγt, IL-17A, and IL-17F, as well as the phosphorylation of Stat3. Although the ligation of Fas results in caspase-8 cleavage and ERK1/2 phosphorylation, inhibitors for caspase-8 and MEK have no effect on the expressions of RORγt, IL-17A, and IL-17F. The results suggest that the Fas signal favors the Th17-phenotypic features of human T cells through the caspase-1/Stat3 signaling pathway. |
| Databáze: | OpenAIRE |
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