Tumor Necrosis Factor (TNF) and Rheumatoid Arthritis

Tumor necrosis factor (TNF) is a substance produced by cells in your immune system that has many effects in promoting the inflammatory process. It is produced chiefly by macrophages, a type of white blood cell, but can be produced by other cells as well. TNF is a major cause of the excess inflammation that drives rheumatoid arthritis (RA).

Tumor Necrosis Factor in the Immune Response

TNF is a natural part of the body's immune response to tumor cells, bacteria, and viruses. It plays a part both in acute reactions and systemic inflammation. Cells release it when they detect a specific substance (an antigen) to which they have become sensitized.

TNF is a cytokine, a signaling protein. Cytokines are chemical substances which deliver messages between cells in the body. They play a part in many biological processes, including:

• Cell proliferation
• Apoptosis, the normal process of the death of a cell
• Lipid (fat) metabolism
• Coagulation, or formation of blood clots

Tumor Necrosis Factor and Rheumatoid Arthritis

TNF may be produced in excess or inappropriately in different disease processes. This can result in ongoing inflammation and other destructive symptoms, and this can be seen in diseases like cancer and insulin resistance (diabetes and pre-diabetes).

As for RA and other autoimmune diseases, tumor necrosis factor-alpha is one of the most important cytokines involved through its entanglement in the cascade of inflammatory reactions.

TNF Inhibitor Drugs

People with health conditions such as rheumatoid arthritis, psoriatic arthritis, and Crohn's disease may be treated with TNF inhibitor drugs (also called blockers). These drugs bind to tumor necrosis factor-alpha, rendering it inactive. This interferes with inflammatory activity and suppresses your immune system.

For people with rheumatoid arthritis, this can decrease joint damage. The first drug was approved in 1998 and more have been developed. They are in the class of biologic drugs, which are medications that target molecules on cells of the immune system.

TNF inhibitor drugs include:

• Enbrel (etanercept)
• Remicade (infliximab)
• Humira (adalimumab)
• Simponi (golimumab)
• Cimzia (certolizumab pegol)

In RA, TNF inhibitor drugs are usually tried if first-line disease-modifying anti-rheumatic drugs (DMARDs) alone haven't provided enough relief.

Using TNF Inhibitors

TNF inhibitors are not taken orally. You must inject them under your skin or into your vein, usually in your thigh or abdomen. According to patient reports, changes in your symptoms begin to occur after two or three doses.

If your healthcare provider prescribes an injectable TNF blocker, you will be taught how to inject it yourself so you won't have to go to the healthcare provider's office each time.

If your healthcare provider prescribes infliximab or golimumab, you will have to go to an infusion center or a healthcare provider's office for up to three hours to receive your treatment. These drugs are not injectable.

Side Effects

TNF blockers can cause side effects. The most common is an injection site reaction, which is usually a localized rash accompanied by a burning sensation or itching.

Also, because TNF blockers suppress your immune system, the drugs raise patients' risk for a wide variety of "opportunistic pathogens," infectious organisms that don't normally sicken healthy people but can cause illness in those with a compromised immune system. These pathogens can be viral, bacterial, mycobacterial, parasitic, or fungal, and the infections can be serious and life-threatening.

People older than 65 seem to be at most risk, as well as people taking concommitant (additional) immunosuppressant medications.

Your healthcare provider will guide you on the benefits, risks, and side effects of TNF blockers, and determine what steps may be necessary to monitor you for infections as you receive treatment.