scholarly journals Suppressors of Cytokine Signaling 3 Expression in Eosinophils: Regulation by PGE2and Th2 Cytokines

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Esther López ◽  
María Paz Zafra ◽  
Beatriz Sastre ◽  
Cristina Gámez ◽  
Mar Fernández-Nieto ◽  
...  
Keyword(s):  
Human Peripheral Blood ◽  
Th2 Cells ◽  
Cytokine Signaling ◽  
Prostaglandin E ◽  
Th2 Cytokines ◽  
Eosinophilic Bronchitis ◽  
Socs Proteins ◽  
Suppressors Of Cytokine Signaling ◽  
Blood Eosinophils ◽  
Socs3 Protein

Asthma and nonasthmatic eosinophilic bronchitis (NAEB) are respiratory disorders characterized by a predominance of Th2 cells and eosinophilic inflammation. Suppressors of cytokine signaling (SOCS) proteins play an important role in Th2-mediated allergic responses through control of the balance between Th1 and Th2 cells, particularly, SOCS3 and SOCS5. The aim of this study was to analyze SOCS expression in human peripheral blood eosinophils from patients with asthma, NAEB and healthy controls. SOCS expression in eosinophils from subjects was demonstrated by different techniques. Results showed that expression of SOCS3 in eosinophils and CD4 T cells from patients was higher than in healthy subjects. In addition, we demonstrated that prostaglandin E2(PGE2) and Th2 cytokines are able to upregulate SOCS3 production in eosinophils and attenuate its degranulation. In conclusion, eosinophils are able to transcribe and translate SOCS3 protein and can contribute to the regulation of the Th1/Th2 balance through SOCS3 production.

scholarly journals SOCS-3 Is Tyrosine Phosphorylated in Response to Interleukin-2 and Suppresses STAT5 Phosphorylation and Lymphocyte Proliferation

1999 ◽  
Vol 19 (7) ◽  
pp. 4980-4988 ◽  
Author(s):  
Solomon J. Cohney ◽  
David Sanden ◽  
Nicholas A. Cacalano ◽  
Akihiko Yoshimura ◽  
Alice Mui ◽  
...  
Keyword(s):  
T Cells ◽  
Tyrosine Phosphorylation ◽  
Human Peripheral Blood ◽  
Interleukin 2 ◽  
Peripheral Blood Lymphocytes ◽  
Cytokine Signaling ◽  
Socs Proteins ◽  
T Cell Lines ◽  
Receptor Beta

ABSTRACT Members of the recently discovered SOCS/CIS/SSI family have been proposed as regulators of cytokine signaling, and while targets and mechanisms have been suggested for some family members, the precise role of these proteins remains to be defined. To date no SOCS proteins have been specifically implicated in interleukin-2 (IL-2) signaling in T cells. Here we report SOCS-3 expression in response to IL-2 in both T-cell lines and human peripheral blood lymphocytes. SOCS-3 protein was detectable as early as 30 min following IL-2 stimulation, while CIS was seen only at low levels after 2 h. Unlike CIS, SOCS-3 was rapidly tyrosine phosphorylated in response to IL-2. Tyrosine phosphorylation of SOCS-3 was observed upon coexpression with Jak1 and Jak2 but only weakly with Jak3. In these experiments, SOCS-3 associated with Jak1 and inhibited Jak1 phosphorylation, and this inhibition was markedly enhanced by the presence of IL-2 receptor beta chain (IL-2Rβ). Moreover, following IL-2 stimulation of T cells, SOCS-3 was able to interact with the IL-2 receptor complex, and in particular tyrosine phosphorylated Jak1 and IL-2Rβ. Additionally, in lymphocytes expressing SOCS-3 but not CIS, IL-2-induced tyrosine phosphorylation of STAT5b was markedly reduced, while there was only a weak effect on IL-3-mediated STAT5b tyrosine phosphorylation. Finally, proliferation induced by both IL-2- and IL-3 was significantly inhibited in the presence of SOCS-3. The findings suggest that when SOCS-3 is rapidly induced by IL-2 in T cells, it acts to inhibit IL-2 responses in a classical negative feedback loop.

Suppressors of cytokine signaling (SOCS) proteins in inflammatory bone disorders

Bone ◽  
2020 ◽  
Vol 140 ◽  
pp. 115538
Author(s):  
Mariana Rates Gonzaga Santos ◽  
Celso M. Queiroz-Junior ◽  
Mila Fernandes Moreira Madeira ◽  
Fabiana Simão Machado
Keyword(s):  
Cytokine Signaling ◽  
Bone Disorders ◽  
Socs Proteins ◽  
Suppressors Of Cytokine Signaling

scholarly journals Suppressors of Cytokine Signaling (SOCS) Proteins and JAK/STAT Pathways

2011 ◽  
Vol 31 (5) ◽  
pp. 980-985 ◽  
Author(s):  
Taiga Tamiya ◽  
Ikko Kashiwagi ◽  
Reiko Takahashi ◽  
Hideo Yasukawa ◽  
Akihiko Yoshimura
Keyword(s):  
Cytokine Signaling ◽  
Socs Proteins ◽  
Suppressors Of Cytokine Signaling

scholarly journals Leishmania donovaniPrevents Oxidative Burst-mediated Apoptosis of Host Macrophages through Selective Induction of Suppressors of Cytokine Signaling (SOCS) Proteins

2013 ◽  
Vol 289 (2) ◽  
pp. 1092-1105 ◽  
Author(s):  
Supriya Srivastav ◽  
Writoban Basu Ball ◽  
Purnima Gupta ◽  
Jayeeta Giri ◽  
Anindita Ukil ◽  
...  
Keyword(s):  
Oxidative Burst ◽  
Cytokine Signaling ◽  
Socs Proteins ◽  
Suppressors Of Cytokine Signaling

scholarly journals Gene Expression Profiling in Lungs of Chronic Asthmatic Mice Treated with Galectin-3: Downregulation of Inflammatory and Regulatory Genes

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Esther López ◽  
M. Paz Zafra ◽  
Beatriz Sastre ◽  
Cristina Gámez ◽  
Carlos Lahoz ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Allergic Inflammation ◽  
Immunohistochemical Analysis ◽  
Th2 Cells ◽  
Cytokine Signaling ◽  
Eosinophilic Inflammation ◽  
Rt Pcr ◽  
Socs3 Expression ◽  
Galectin 3 ◽  
Socs Proteins

Background. Asthma is a disorder characterized by a predominance of Th2 cells and eosinophilic inflammation. Suppressors of cytokine signaling (SOCS) proteins act as negative regulators of cytokine signaling. In particular, SOCS1 and SOCS3 play an important role in immune response by controlling the balance between Th1 and Th2 cells. In a previous study, we demonstrated that treatment of chronic asthmatic mice with gene therapy using plasmid encoding galectin-3 (Gal-3) led to an improvement in Th2 allergic inflammation.Methods. Using a microarray approach, this study endeavored to evaluate the changes produced by therapeutic Gal-3 delivered by gene therapy in a well-characterized mouse model of chronic airway inflammation. Results were confirmed by real-time RT-PCR, Western blot and immunohistochemical analysis.Results. We identify a set of genes involved in different pathways whose expression is coordinately decreased/increased in mice treated with Gal-3 gene therapy. We report a correlation between Gal-3 treatment and inhibition of SOCS1 and SOCS3 expression in lungs.Conclusion. These results suggest that negative regulation of SOCS1 and 3 following Gal-3 treatment could be a valuable therapeutic approach in allergic disease.

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