Endogenous chemical mediators or autacoids play key roles in controlling inflammation and its programmed resolution.
Chemokines, as well as other inflammatory mediators, appear to play key roles in the pathogenesis of RA, and the co-ordinated production of chemokines and proinflammatory cytokines is probably important in the orchestration of the inflammatory responses observed in patients with RA [ 1- 4].
In addition, rapidly generated lipid mediators play a key role in orchestration of inflammation and its resolution (Serhan et al, 2008).
Cytokines such as IL-1 and type I IFNs and lipid mediators, such as eicosanoids, play key roles in regulating the balance between host-detrimental and host-beneficial immune responses and as such represent important targets for immunologic intervention.
By quantitatively identifying, the most important mediator genes are seemingly unimportant but play key roles in maintaining communication between disease genes and these mediators are not hubs in PPI.
Various cytokines are known to play key roles as mediators of RA progression.
Caspase-3 is a critical enzymatic mediator of PCD and appears to play key roles in the late initiation and early execution phases of apoptosis.
Cytokines are known to play key roles as the mediators of RA progression.
Inflammatory mediators, such as PGE2, NO, IL-1, and TNF-α, play key roles in the progression of cartilage destruction in OA [ 28, 29].
Activator Mediator binding alters Mediator structure, and these activator-induced structural shifts appear to play key roles in regulating transcription.
