A study published in the Journal of Experimental Medicine finds that removing an immune system signaling protein in mice prevented the animals from developing a lupus-like condition.
In this particular animal model of lupus, the mice are exposes to pristane which causes a lupus-like condition in the animals. Researchers at Washington University School of Medicine in St. Louis and the National Institutes of Health created a genetically modified line of mice that lacked SLAM-associated protein (SAP). Both previous animal and human studies have suggested that SAP plays an important role in lupus.
The modified mice did not develop the lupus-like condition when exposed to pristane, but otherwise their immune system was not seriously compromised. In a press release announcing the publication of the group’s findings, lead researcher Stanford Peng said,
What’s perhaps most exciting is that normal immune system functions were still largely intact in the experimental mice that lacked SAP. Other immune system proteins are potential targets for new autoimmune disease treatments, but they all affect large portions of the immune system, making weakened immune function a potential side effect of any new drug. Targeting SAP for treatment may avoid that risk.
The lack of SAP appears to interfere with communication between immune system T and B cells. That finding in itself could provide important new information about the immune system according to Peng,
We know a lot of molecules that are important to the activation of T and B cells, but we have never understood what was important for their interaction. SAP may give us an important first insight into how these interactions occur.
Peng now plans to test how the genetically modified mice fare in other mouse models of lupus.
Source:
Lack of immune system protein prevents lupus-like condition in mice. Press Release, Washington University School of Medicine, July 8, 2004.