A novel type-1 cytokine receptor from fish involved in the Janus kinase/Signal transducers and activators of transcription (Jak/STAT) signal pathway

2007 ◽  
Vol 44 (13) ◽  
pp. 3355-3363 ◽  
Author(s):  
Mudjekeewis D. Santos ◽  
Motoshige Yasuike ◽  
Hidehiro Kondo ◽  
Ikuo Hirono ◽  
Takashi Aoki
2019 ◽  
Vol 19 (5) ◽  
pp. 656-664
Author(s):  
Yunjuan Zhao ◽  
Yunliang Xie ◽  
Wangen Li

Background: Type 1 diabetes is a T cell-mediated autoimmune disease. Interferon γ plays a critical role in the pathogenesis of type 1 diabetes. Signal transducer and activator of transcription transduces type I interferon cytokines in T cells, leading to Th1 cell differentiation and production of interferon γ. Recent studies suggest that liraglutide reduces the plasma concentration of C-reative protein in patients with type 1 diabetes and protects β cell function in the non-obese diabetic mouse. Objective: The study aimed to explore the effect of glucagon-like peptide-1 analogue on interferon γ production and the underlying signaling pathway in vitro. Methods: Jurkat E6-1 cells were intervened with different concentrations of glucose and liraglutide during different time periods. Protein was extracted from Jurkat E6-1 cells. The target proteins (total and activated Janus kinase 2, signal transducers and activators of transcription 4 and interferon γ) were detected by Western blot. Results: Glucose stimulates interferon γ expression and activates Janus kinase 2/signal transducers and activators of transcription 4 signaling pathway in Jurkat E6-1 cells in a concentration and timedependent manner. Under high glucose condition, liraglutide inhibits interferon γ expression and Janus kinase 2/signal transducers and activators of transcription 4 signaling pathway in Jurkat E6-1 cells in a concentration and time-dependent manner. The Janus kinase responsible for liraglutide-inhibited signal transducers and activators of transcription 4 phosphorylation is Janus kinase 2, which is also required for the interferon γ induction. Finally, we demonstrated that under high glucose condition, liraglutide inhibits interferon γ expression via Janus kinase 2/signal transducers and activators of transcription 4 signaling pathway in Jurkat E6-1 cells. Conclusion: Liraglutide inhibits Jurkat E6-1 cells to produce interferon γ via the Janus kinase/signal transducers and activators of transcription signaling pathway under high glucose condition, which implies its potential in the immunoregulatory effect of type 1 diabetes.


2005 ◽  
Vol 16 (6) ◽  
pp. 1673-1683 ◽  
Author(s):  
Purificación Hernández-Vargas ◽  
Oscar López-Franco ◽  
Guillermo Sanjuán ◽  
Mónica Rupérez ◽  
Guadalupe Ortiz-Muñoz ◽  
...  

Blood ◽  
2012 ◽  
Vol 120 (18) ◽  
pp. 3718-3728 ◽  
Author(s):  
M. Pilar Gil ◽  
Mickaël J. Y. Ploquin ◽  
Wendy T. Watford ◽  
Seung-Hwan Lee ◽  
Kwangsin Kim ◽  
...  

Abstract Type 1 IFNs can conditionally activate all of the signal transducers and activators of transcription molecules (STATs), including STAT4. The best-characterized signaling pathways use STAT1, however, and type 1 IFN inhibition of cell proliferation is STAT1 dependent. We report that type 1 IFNs can basally stimulate STAT1- and STAT4-dependent effects in CD8 T cells, but that CD8 T cells responding to infections of mice with lymphocytic choriomenigitis virus have elevated STAT4 and lower STAT1 expression with significant consequences for modifying the effects of type 1 IFN exposure. The phenotype was associated with preferential type 1 IFN activation of STAT4 compared with STAT1. Stimulation through the TCR induced elevated STAT4 expression, and STAT4 was required for peak expansion of antigen-specific CD8 T cells, low STAT1 levels, and resistance to type 1 IFN-mediated inhibition of proliferation. Thus, a mechanism is discovered for regulating the consequences of type 1 IFN exposure in CD8 T cells, with STAT4 acting as a key molecule in driving optimal antigen-specific responses and overcoming STAT1-dependent inhibition of proliferation.


Circulation ◽  
2003 ◽  
Vol 107 (6) ◽  
pp. 798-802 ◽  
Author(s):  
Edith K. Podewski ◽  
Denise Hilfiker-Kleiner ◽  
Andres Hilfiker ◽  
Henning Morawietz ◽  
Artur Lichtenberg ◽  
...  

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