Supplemental Material for Cross-Species Evidence for the Role of Interleukin-33 in Depression Risk

2016 ◽  
Vol 125 (4) ◽  
pp. 482-494 ◽  
Author(s):  
Anastacia Y. Kudinova ◽  
Terrence Deak ◽  
Cara M. Hueston ◽  
John E. McGeary ◽  
Valerie S. Knopik ◽  
...  

2017 ◽  
Vol 33 (9) ◽  
pp. 708-711 ◽  
Author(s):  
Cenk Nayki ◽  
Umit Nayki ◽  
Mehmet Kulhan ◽  
Mustafa Ozkaraca ◽  
Serdar Altun ◽  
...  
Keyword(s):  

2013 ◽  
Vol 4 (1) ◽  
pp. 111-114 ◽  
Author(s):  
Rania M. Abdel Hay ◽  
Noha F. Ibrahim ◽  
Dina Metwally ◽  
Laila A. Rashed

2019 ◽  
Vol 20 (20) ◽  
pp. 5226 ◽  
Author(s):  
Alessandro Allegra ◽  
Vanessa Innao ◽  
Gennaro Tartarisco ◽  
Giovanni Pioggia ◽  
Marco Casciaro ◽  
...  

Interleukin (IL)-33 is a chromatin-related nuclear interleukin that is a component of IL-1 family. IL-33 production augments the course of inflammation after cell damage or death. It is discharged into the extracellular space. IL-33 is regarded as an “alarmin” able to stimulate several effectors of the immune system, regulating numerous immune responses comprising cancer immune reactions. IL-33 has been demonstrated to influence tumorigenesis. However, as far as this cytokine is concerned, we are faced with what has sometimes been defined as the IL-33 paradox. Several studies have demonstrated a relevant role of IL-33 to numerous malignancies, where it may have pro- and—less frequently—antitumorigenic actions. In the field of hematological malignancies, the role of IL-33 seems even more complex. Although we can affirm the existence of a negative role of IL-33 in Chronic myelogenos leukemia (CML) and in lymphoproliferative diseases and a positive role in pathologies such as Acute myeloid leukemia (AML), the action of IL-33 seems to be multiple and sometimes contradictory within the same pathology. In the future, we will have to learn to govern the negative aspects of activating the IL-33/ST2 axis and exploit the positive ones.


2019 ◽  
Vol 32 (5) ◽  
Author(s):  
Mohammed Abu El‐Hamd ◽  
Hanan Abdel Rady Assaf ◽  
Ahmed Sedky ◽  
Shrouk Haggag Mohammad

2011 ◽  
Vol 54 ◽  
pp. S53
Author(s):  
T. Mchedlidze ◽  
S. Pflanz ◽  
M.F. Neurath ◽  
S. Wirtz

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Qing Zhao ◽  
Guangjie Chen

Interleukin-33 (IL-33) is a new cytokine of interleukin-1 family, whose specific receptor is ST2. IL-33 exerts its functions via its target cells and plays different roles in diseases. ST2 deletion and exclusion of IL-33/ST2 axis are accompanied by enhanced susceptibility to dominantly T cell-mediated organ-specific autoimmune diseases. It has been reported that IL-33/ST2 pathway plays a key role in host defense and immune regulation in inflammatory and infectious diseases. This review focuses on new findings in the roles of IL-33 and ST2 in several kinds of T cell-mediated autoimmune diseases.


2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Juan Wang ◽  
Pingwei Zhao ◽  
Hui Guo ◽  
Xiguang Sun ◽  
Zhenyu Jiang ◽  
...  

Interleukin-33 (IL-33) is associated with the development of Th2 responses. This study examined the potential role of IL-33 in the pathogenic process of chronic hepatitis C (CHC) in Chinese patients. The levels of serum IL-33 and sST2 in 154 patients with CHC, 24 with spontaneously resolved HCV (SR-HCV) infection and 20 healthy controls (HC), were analyzed by ELISA. The concentrations of serum IL-2, IFN-γ, TNF-α, IL-4, IL-6, and IL-10, HCV loads, ALT, AST, and HCV-Ab were measured. We found that the levels of serum IL-33 in CHC patients were significantly higher than those of SR-HCV and HC but decreased after treatment with interferon for 12 weeks. More importantly, the levels of serum IL-33 were correlated with the concentrations of ALT and AST in CHC patients. The levels of serum sST2, as a decoy receptor of IL-33, were significantly higher in CHC and SR-CHC patients than those in HC, and there was no correlation between the levels of serum sST2 and IL-33. The concentrations of serum IFN-γ and IL-6 in CHC patients were significantly lower than those of SR-HCV. These data suggest that IL-33 may be a pathogenic factor contributing to CHC-related liver injury.


2020 ◽  
Vol 11 (2) ◽  
pp. 120-125 ◽  
Author(s):  
Ilona Paulauskaite ◽  
Audrone Eidukaite ◽  
Odilija Rudzevičiene

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