Interleukin-6 and interleukin-11 support human osteoclast formation by a RANKL-independent mechanism

Bone ◽  
2002 ◽  
Author(s):  
O Kudo
Bone ◽  
2003 ◽  
Vol 32 (1) ◽  
pp. 1-7 ◽  
Author(s):  
O Kudo ◽  
A Sabokbar ◽  
A Pocock ◽  
I Itonaga ◽  
Y Fujikawa ◽  
...  

1997 ◽  
Vol 40 (6) ◽  
pp. 1096-1105 ◽  
Author(s):  
Hideyuki Okamoto ◽  
Masahiro Yamamura ◽  
Yoshitaka Morita ◽  
Seishi Harada ◽  
Hirofumi Makino ◽  
...  

Arthritis ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Misato Hashizume ◽  
Masahiko Mihara

Several clinical studies have demonstrated that the humanized anti-interleukin-6 (IL-6) receptor antibody tocilizumab (TCZ) improves clinical symptoms and prevents progression of joint destruction in rheumatoid arthritis (RA). However, the precise mechanism by which IL-6 blockade leads to the improvement of RA is not well understood. IL-6 promotes synovitis by inducing neovascularization, infiltration of inflammatory cells, and synovial hyperplasia. IL-6 causes bone resorption by inducing osteoclast formation via the induction of RANKL in synovial cells, and cartilage degeneration by producing matrix metalloproteinases (MMPs) in synovial cells and chondrocytes. Moreover, IL-6 is involved in autoimmunity by altering the balance between Th17 cells and Treg. IL-6 also acts on changing lipid concentrations in blood and on inducing the production of hepcidin which causes iron-deficient anemia. In conclusion, IL-6 is a major player in the pathogenesis of RA, and current evidence indicates that the blockade of IL-6 is a beneficial therapy for RA patients.


Author(s):  
Juliane Lokau ◽  
Marieke Wandel ◽  
Christoph Garbers
Keyword(s):  

2020 ◽  
Vol 16 (10) ◽  
pp. 2357-2362 ◽  
Author(s):  
Anissa A. Widjaja ◽  
Sonia P. Chothani ◽  
Stuart A. Cook
Keyword(s):  

2014 ◽  
Vol 81 (9) ◽  
pp. 871-875 ◽  
Author(s):  
Juan Liang ◽  
Zhiyu Lei ◽  
Xiaojun Xu ◽  
Ning Zhao ◽  
Hua Song ◽  
...  

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