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False alarm can spark autoimmune disease

December 7, 2011

An unchecked signaling mechanism could be the reason the immune system sometimes goes off track to attack the body’s own cells.
The problem lies in what are called innate immune cells, the first responders to infection, says Cynthia Leifer, assistant professor of microbiology and immunology at Cornell University. The findings may open the door for new therapies for diseases like lupus and arthritis.

“Innate immune cells have internal watchdogs called TLR-9 receptors that set off alarms whenever they encounter invaders. They look for general classifying patterns (in DNA) to determine whether something is a virus, bacterium, protozoan, or part of self.”

But as reported in the European Journal of Immunology, some of these patterns exist both in invading organisms and the body’s own cells, so mistakes can arise.

“We are mapping the critical regulatory mechanisms that keep these receptors from responding to self-DNA so that we can know if and how they predispose people to autoimmune disorders when they fail,” Leifer says.

Innate immune cells engulf things that look dangerous, tear them open, and release their components, including DNA. When TLR-9 receptors see DNA that identifies microbes, they send a signal to fire up more immune-system activity, including inflammation and the creation of antibodies. But before a receptor can work, enzymes in the cell must prepare it by chopping off part of the receptor molecule and leaving a part that can bind to microbe DNA.

From there, Leifer believes it’s a numbers game. If too many receptors are prepared, they may respond to the small amount of self-DNA that makes its way into immune cells, triggering an autoimmune response. So the immune cell has a regulatory mechanism, an enzyme pathway that cuts prepared receptors in a second place.

Read the Full Article Here

Source futurity.org


False alarm can spark autoimmune disease

December 7, 2011

An unchecked signaling mechanism could be the reason the immune system sometimes goes off track to attack the body’s own cells.
The problem lies in what are called innate immune cells, the first responders to infection, says Cynthia Leifer, assistant professor of microbiology and immunology at Cornell University. The findings may open the door for new therapies for diseases like lupus and arthritis.

“Innate immune cells have internal watchdogs called TLR-9 receptors that set off alarms whenever they encounter invaders. They look for general classifying patterns (in DNA) to determine whether something is a virus, bacterium, protozoan, or part of self.”

But as reported in the European Journal of Immunology, some of these patterns exist both in invading organisms and the body’s own cells, so mistakes can arise.

“We are mapping the critical regulatory mechanisms that keep these receptors from responding to self-DNA so that we can know if and how they predispose people to autoimmune disorders when they fail,” Leifer says.

Innate immune cells engulf things that look dangerous, tear them open, and release their components, including DNA. When TLR-9 receptors see DNA that identifies microbes, they send a signal to fire up more immune-system activity, including inflammation and the creation of antibodies. But before a receptor can work, enzymes in the cell must prepare it by chopping off part of the receptor molecule and leaving a part that can bind to microbe DNA.

From there, Leifer believes it’s a numbers game. If too many receptors are prepared, they may respond to the small amount of self-DNA that makes its way into immune cells, triggering an autoimmune response. So the immune cell has a regulatory mechanism, an enzyme pathway that cuts prepared receptors in a second place.

Read the Full Article Here

Source futurity.org



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