الفهرس 
Introduction and RationaleOnly 14 pages are availabe for public view
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Abstract
RA is the most common connective tissue disease affecting approximately 1% of
the population and represents an increasing burden on global health resources.
Survival in RA patients is lower than that of the normal population.
RA is a chronic progressive, systemic inflammatory condition, characterized by
synovial proliferation and symmetric, erosive arthritis of peripheral joints. The
hallmark feature is persistent symmetric polyarthritis (synovitis) that affects the
hands, wrists and feet, although almost all joints may become involved.
Systemic involvement as a part of the disease may cause constitutional symptoms;
rheumatoid nodules, serositis and vasculitis. The severity of RA may fluctuate over
time, but chronic RA most commonly results in the progressive development of
various degrees of joint destruction, deformity, significant decline in functional status
and premature death.
Cytokines which comprise a family of proteins act in concert with specific
cytokine inhibitors and soluble cytokine receptors to regulate the human immune
response. An imbalance in cytokine production or cytokine receptor expression
and/or dysregulation of cytokine process contributes to various pathological
disorders.
IL-33, a member of the IL-1 family, is a ligand for the orphan receptor ST2 (also
known as IL-1RL1). When IL-33 binds to ST2, it enhances inflammatory cytokines
via the activation of nuclear factor-κB (NF-κB) and MAP kinases. Although it was
initially thought that IL-33 was crucial for Th2 cytokine-mediated immune responses,
it is now suggested that, it can overcome to have a role in RA.