The role of soluble interleukin-6 receptor in inflammatory diseases

2005 ◽  
Vol 98 (1) ◽  
pp. 171
Author(s):  
Marcello Maggio ◽  
Shehzad Basaria ◽  
Gian Paolo Ceda ◽  
Graziano Ceresini ◽  
Giorgio Valenti ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Inflammatory Diseases ◽  
Interleukin 6 Receptor

Reply to “The role of soluble interleukin-6 receptor in inflammatory diseases” [Immunol Lett 2005;98(1):171]

2006 ◽  
Vol 105 (1) ◽  
pp. 99-99
Author(s):  
M MICHALOPOULOU ◽  
C NIKOLAOU ◽  
A TAVERNARAKIS ◽  
N ALEXANDRI ◽  
M RENTZOS ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Inflammatory Diseases ◽  
Interleukin 6 Receptor

scholarly journals Inducible microRNA-590-5p inhibits host antiviral response by targeting the soluble interleukin-6 (IL6) receptor

2018 ◽  
Vol 293 (47) ◽  
pp. 18168-18179 ◽  
Author(s):  
Yaqin Zhou ◽  
Zhangchuan Xia ◽  
Zhikui Cheng ◽  
Gang Xu ◽  
Xiaodan Yang ◽  
...  
Keyword(s):  
Viral Infection ◽  
Interleukin 6 ◽  
Underlying Mechanism ◽  
Antiviral Response ◽  
Type I ◽  
Interleukin 6 Receptor ◽  
Important Regulator ◽  
Membrane Bound ◽  
Host Antiviral Response

MicroRNA (miR)-590-5p has been identified as an important regulator of some signaling pathways such as cell proliferation and tumorigenesis. However, little is known about its role during viral infection. Here, we report that miR-590-5p was significantly induced by various viruses and effectively potentiated virus replication in different viral infection systems. Furthermore, miR-590-5p substantially attenuated the virus-induced expression of type I and type III interferons (IFNs) and inflammatory cytokines, resulting in impaired downstream antiviral signaling. Interleukin-6 receptor (IL6R) was identified as a target of miR-590-5p. Interestingly, the role of miR-590-5p in virus-triggered signaling was abolished in IL6R knockout cells, and this could be rescued by restoring the expression of the soluble IL6R (sIL6R) but not the membrane-bound IL6R (mIL6R), suggesting that sIL6R is indispensable for miR-590-5p in modulating the host antiviral response. Furthermore, miR-590-5p down-regulated endogenous sIL6R and mIL6R expression through a translational repression mechanism. These findings thus uncover a previously uncharacterized role and the underlying mechanism of miR-590-5p in the innate immune response to viral infection.

scholarly journals Primary pathologic role of interleukin-6 in rheumatoid arthritis

2013 ◽  
pp. 40-46
Author(s):  
G.L. Bajocchi ◽  
N. Pipitone ◽  
P.L. Boiardi ◽  
C. Salvarani
Keyword(s):  
Rheumatoid Arthritis ◽  
Interleukin 6 ◽  
Cultured Cells ◽  
Inflammatory Diseases ◽  
Acute Phase Reactant ◽  
Therapeutic Benefit ◽  
Phase Iii ◽  
Tnf Alpha ◽  
Proinflammatory Activity

BACKGROUND Interleukin-6 (IL-6) is a polyfunctional cytokine that regulates a very large number of cellular activities. Its implication in acute-phase reactant production by hepatocytes is of particular interest, as is its involvement in chronic inflammatory diseases, mainly rheumatoid arthritis, Crohn’s disease, and Castleman’s disease. Transgenic mice lacking IL-6 expression were completely protected against collagen-induced arthritis, and Tumor Necrosis Factor (TNF-alpha) induces synovial cells to produce IL-6 and their proliferation. However, there is still some controversies regarding the unique proinflammatory activity of IL-6. Some studies have demonstrated that IL-6 and TNF-alpha may have an opposite effect in synovial cultured cells since IL-6 could represent a negative loop for TNF-alpha induced synovitis. However, phase III studies of rheumatoid arthritis patients treated with anti IL-6 receptor (tocilizumab) indicate an acceptable safety profile relative to the clinical benefit. AIM OF THE STUDY In this review, we summarized the rationale and the main evidence regarding the therapeutic benefit of blocking IL-6 activity in rheumatoid arthritis.

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