scholarly journals Transforming growth factor β 869C/T and interleukin 6 -174G/C polymorphisms relate to the severity and progression of bone-erosive damage detected by ultrasound in rheumatoid arthritis

2011 ◽  
Vol 13 (4) ◽  
pp. R111 ◽  
Author(s):  
Fulvia Ceccarelli ◽  
Carlo Perricone ◽  
Martina Fabris ◽  
Cristiano Alessandri ◽  
Annamaria Iagnocco ◽  
...  
2007 ◽  
Vol 82 (2) ◽  
pp. 354-360 ◽  
Author(s):  
Shih-Jen Liu ◽  
Jy-Ping Tsai ◽  
Chia-Rui Shen ◽  
Yuh-Pyng Sher ◽  
Chia-Ling Hsieh ◽  
...  

2014 ◽  
Vol 1 (1) ◽  
pp. 8-11
Author(s):  
Bilal Bengana ◽  
◽  
Samy Slimani ◽  
Bachir Hachemi ◽  
◽  
...  

Rheumatoid arthritis is a chronic systemic inflammatory disease of unknown cause. An external trigger (eg, cigarette smoking, infection, or trauma) that triggers an autoimmune reaction, leading to synovial hypertrophy and chronic joint inflammation along with the potential for extra-articular manifestations, is theorized to occur in genetically susceptible individuals. Several genes are implicated including class II major histocompatibility complex genes, PTPN22, and C5-TRAF1. Adaptive and innate immune responses in the synovium have been implicated in the pathogenesis of RA. Evidence of autoimmunity, including high serum levels of autoantibodies such as rheumatoid factors and anticitrullinated peptide antibodies, can be present for many years before the onset of clinical arthritis. Although inciting factors have yet to be identified, the presence and activity of a number of proinflammatory chemokines and cytokines have established roles in disease pathogenesis. The activation and infiltration of T cells and macrophages in the synovium result in the production of interleukin-1, -2, -6, -8, -10, -17; tumor necrosis factor-α (TNF-α); platelet-derived growth factor; insulin-like growth factor; and transforming growth factor β (TGF β). These effector molecules are implicated in synovial tissue inflammation and proliferation, cartilage and bone destruction, and systemic effects.


2013 ◽  
Vol 36 (4) ◽  
pp. 344-347
Author(s):  
Christopher L. Hallemeier ◽  
Matt J. Iott ◽  
James A. Martenson ◽  
Michael G. Haddock ◽  
Xinghua (Cathy) Zhao ◽  
...  

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