Stories about: immune surveillance

Link found between chronic inflammation, autoimmune disorders and “false alarms”

Viruses (pictured here) have a genetic signature that a receptor called MDA5 recognizes. But when MDA5 confuses the body's own genetic material with that of a virus, disease ensues.
Viruses have a genetic signature that a human receptor called MDA5 recognizes, causing the immune system to attack. But when MDA5 confuses the body’s own genetic material for that of a virus, disease ensues.

The human body’s innate immune system employs a variety of “sensors” for identifying foreign invaders such as viruses. One such viral sensor is a receptor called MDA5, found in every cell of the body.

Inside each cell, MDA5 constantly scans genetic material, checking if it’s native to the body or not. As soon as MDA5 identifies the genetic signature of a viral invader, it trips a system-wide alarm, triggering a cascade of immune activity to neutralize the threat.

But if a genetic mutation to MDA5 causes it to confuse some of the body’s own genetic material for being foreign, “false alarms” can lead to unchecked inflammation and disease. Scientists from Boston Children’s Hospital have discovered a new link between MDA5’s ability to discriminate between “self” and “non-self” genetic material — called RNA duplexes — and a spectrum of autoimmune disorders.

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Immune system to Epstein-Barr virus-fueled cancers: “I’ve got an eye on you”

In the vast majority of us, the Epstein-Barr virus (above) causes mild illness and never bothers us again. However, it can lay dormant in small numbers of B cells for years, waking up if the immune surveillance keeping it in check is broken and fueling lymphomas. (NCI)

Some 90 percent of us are exposed to the Epstein-Barr virus (EBV) at some point in our lives. While the immune system’s T cells rapidly clear most EBV-infected B cells, about one in a million infected cells escapes destruction. Within these cells, the virus enters a latent phase, kept in check by the watchful eye of so-called memory T cells.

This uneasy relationship usually holds steady for the rest of our lives, unless something suppresses the immune system – such as infection with HIV or use of anti-rejection drugs after a transplant – and breaks the surveillance. The virus can then reawaken and drive the development of certain B cell cancers.

How do our T cells keep their watch?

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