Macrophage Receptor Triggers Lung Overreaction to Flu Infection

In the current study, investigators at Imperial College (London, UK;) used a mouse model that had been genetically engineered to lack the gene for CD200 to examine the effect of this defect on the animal's response to influenza infection.

Results published in the July 27, 2008, online edition of the journal Nature Immunology revealed that mice lacking CD200 had more macrophage activity and enhanced sensitivity to influenza infection, which led to delayed resolution of inflammation and, ultimately, death. The administration of agonists that bound CD200R, however, prevented inflammatory lung disease.

Senior author Dr. Tracy Hussell, professor of inflammatory disease at Imperial College said, "The immune system is very sophisticated and much of the time it does a fantastic job of fighting infection, but it has the ability to cause a lot of damage when it overreacts. Our new research is still in its early stages, but these findings suggest that it could be possible to prevent the immune system going into overdrive, and limit the unnecessary damage this can cause.”

Therapy based on stimulating the CD200-CD200R axis would be effective even if the flu virus mutated, because it targets the body's overreaction to the virus rather than the virus itself.

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