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RA is characterized by a systemic inflammatory state, in which immune cells and soluble mediators play a crucial role.

These inflammatory processes resemble those in other chronic inflammatory diseases, such as atherosclerosis.

Among several mediators, the pro-inflammatory cytokine TNF-α has been shown as a crucial factor to induce atherosclerosis in RA patients.

RA is a chronic inflammatory disease, which affects ∼1% of the population world wide [1–3]. However, RA is characterized by a systemic inflammatory state, involving several organs, including joints, skin, eyes, lung and blood vessels [4].

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One of his victims, who cannot be named for legal reasons, sobbed in the public gallery and shook her head, as Meldrum was told his 12 month prison sentence would be suspended for two years.

The chronic systemic inflammation in RA can be considered as an independent risk factor for the development of atherosclerosis, and represents an important field to investigate the reasons of the increase of acute cardiovascular events in RA.

In the present review, we focused on several mediators of autoimmunity, inflammation and endothelial dysfunction, which can be considered the most promising targets to prevent atherogenesis in RA.

Stimulation of PMN with SSCM led to a marked increase in PMN adhesion to h CMEC/D3, as compared to CCM.

PMN adhesion was abolished with neutralizing antibodies to either β2 (CD18), α Human SSCM up-regulates PMN pro-adhesive phenotype and promotes PMN adhesion to cerebrovascular endothelial cells through a β2-integrin-ICAM-1-dependent mechanism.


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