How do anti-TNF biologics work?

Question: I became interested in immunology when I was diagnosed with Rheumatoid Arthritis (and Crohn's disease) I have taken several anti-TNF biologics. Could you please illustrate how they work? Thanks!

Asked by: soundofaspark

Insight: The pathogenesis of Crohn’s disease and rheumatoid arthritis is complex.
If  I were to over simply it, I’d think of the disease as a type IV hypersensitivity in which the body is reacting to commensal bacteria in Crohns disease and type II hypersensitivity in which the body is reacting to self antigens in Rheumatoid Arthritis.

One of the principal cytokines secreted by activated macrophages is TNF-a. TNF-a is an inducer of a local inflammatory response that helps to contain infections.

Answer: Think of TNF-a as a key. It’s unlocks the door to many inflammatory processes, some of which may be harmful. Think of TNF-a receptor as the key hole.

Some anti-TNF biologics like Infliximab bind to the key and make them look funny! This prevents the effective binding of TNF-α with its receptors.

Other anti-TNF biologics such as Etanercept look like the key hole. They bind to it and prevent TNF-a to bind to the real key hole. It reduces the effect of naturally present TNF, and hence is a TNF inhibitor, functioning as a decoy receptor that binds to TNF. This is what complex terms like “soluble proteins that mimic the receptor” mean.

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