Autoimmune diseases are characterized by the body’s immune reponses being directed against its own tissues, causing prolonged inflammation and subsequent tissue destruction. Autoimmune disorders can cause immune-responsive cells to attack the linings of the joints – resulting in rheumatoid arthritis (RA). The pathogenesis of RA is a complex process, involving synovial cell proliferation and fibrosis, pannus formation and cartilage and bone erosion. This process is mediated by an interdependent network of cytokines, prostanoids and proteolytic enzymes. Proinflammatory cytokines, such as interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha), are central mediators in RA. Inflammatory cells release enzymes that may digest bone and cartilage. The involved joint can lose its shape and alignment, resulting in pain and loss of movement. Treatments attempt to control inflammatory symptoms, decrease pain, prevent or control joint damange and prevent loss of function. Identification of new anti-inflammatory therapeutics are currently high on the agenda. More specifically; non-steroidals, COX-2 inhibitors and salicylates are required for an ever expanding market.

What researchers are currently using:

Currently, experimentation in the lab involves targeting immune cells and dampening their activity. Assessment methods include cell activity assays in static well plate settings, PCR of the relevant genes induced and toxicity screens. Performing experiments in isolation independent of hte key signals that drive and influence inflammation will restrict the value of the data obtained.