October 12, 2017 / All Stories

Gone rogue: what happens when cells say the wrong thing

An exploration of the immune system and the role cells play in inflammatory immune diseases.

Dendritic cells help analyze threats in the body and share information with other cells.

Diving deeper for answers

The body constantly fights off “foreign” invaders that can cause infection or harm. On the surface we may see the effects of that fight, but it's not until we dive beneath that we see a clear view of the immune system and the multitude of players involved.

Shining more light on the inner workings of the immune system may help scientists to define the future of immune-mediated diseases.

Uncovering a complex network

Inside the body, proteins, cells and tissues work together as our “immune system.” Like a giant chat room, they communicate constantly to monitor for threats, tell each other where to go and activate defenses when risks are detected.

On a mission to protect the body

Always alert, white blood cells, or leukocytes, travel through the body reacting to warning signals about potential threats. When duty calls, they create healthy inflammation that protects the body when a threat is identified. T-cells, B-cells, dendritic cells and macrophages -- different types of leukocytes -- play unique roles in the process.

White blood cells travel through the body sending warnings about potential threats. Learn more about their unique role:

Signaling for support

But white blood cells can’t do it all alone. They need the help of cytokines, tiny helper proteins that send messages from one cell to another, to get the job done.

But what happens if one cytokine starts saying the wrong thing?

Mapping the chain reaction

While some cytokines create inflammation, others sound the alarm to raise defenses. Let’s dive a little deeper to see how it might play out with one specific cytokine: interleukin (IL) 23.

IL-23 alerts T-cells, telling them to produce more of cytokine IL-17, which recruits other white blood cells to the site of inflammation1.

But if IL-23 goes rogue, it changes the message in the chain and puts IL-17 into overdrive. The result? Too much inflammation that harms the body instead of protecting it. This increased inflammation plays a role in immune-mediated diseases like psoriasis, Crohn’s disease and rheumatoid arthritis.

IL-23 tells T-cells to produce IL-17 when it’s necessary to protect the body.
But if IL-23 sends the wrong message, it can trigger production of too much IL-17, resulting in too much inflammation.

Entering uncharted territory

This clearer picture of immune pathways like IL-23 is opening new doors for the research community to explore ways of targeting and treating immune-mediated diseases.

As scientists and researchers have spent the past 15-20 years discovering answers on the role IL-23 plays, they’re eager to unlock the potential of those answers.

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Florian Dieckmann
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  1. Yoichiro Iwakura, Harumichi Ishigame (May 2006). “The IL-23/IL-17 axis in inflammation.” J Clin Invest. 116(5): 1218–1222. doi: 10.1172/JCI28508.