Infliximab works by binding specifically to a protein called TNF-α (tumor necrosis factor-alpha), which is released by white blood cells as part of our body’s immune response to infection or invasion by foreign substances. Overproduction of TNF-α can cause inflammation, which can damage tissues, bones, and cartilage, and also cause cell death. When infliximab binds to TNF-α, it blocks its effects, and this reduces inflammation. Increased levels of TNF-alfa have been found in conditions such as rheumatoid arthritis, psoriasis, and ankylosing spondylitis.

Infliximab is called a monoclonal antibody because the definition of monoclonal antibodies is that they bind specifically to a protein – in this case, infliximab binds specifically to TNF-α.

How does infliximab work for ulcerative colitis?

Infliximab blocks the form of TNF-α that exists on cell surfaces, including the membrane lining the bowel surface. This reduces inflammation on the surface of the bowel, which helps the symptoms of ulcerative colitis.

How does infliximab work for rheumatoid arthritis (RA)?

In addition to blocking TNF-α, Infliximab also inhibits other proinflammatory substances such as interleukin 1 (IL-1) and IL-6 gene expression. These are expressed on the surface of osteoclasts (the cells that degrade bone during the process of bone remodeling) and osteoclasts (the cells that lay new bone). IL-1 is also present in the synovial tissue and fluid – the specialized tissue and fluid that keeps the joint well lubricated, and at the same time, provide nutrients to the articular surface. IL-1 appears to play a major role in joint destruction. When infliximab is used to treat RA it reduces levels of IL-1 which reduces synovitis and joint destruction.

How does infliximab work for psoriasis?

High levels of TNF-α are found in the skin lesions and plasma of people with psoriasis and treatment with infliximab reduces these levels, reducing inflammation. TNF-α is also responsible for the characteristic silvery plaques of plaque psoriasis because it speeds up the proliferation of keratinocytes and prevents their death, causing an abundance of them which forms the silvery plaque. Inhibition of TNF-α by infliximab stops this from happening and can significantly improve the appearance of plaques.