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U-M scientists target key cells and signals that trigger pulmonary fibrosis

blood samples from U-M patients with the disease. According to Moore, they found fibrocytes from IPF patients produced three times the normal amount of collagen.

"Fibrocytes have at least six different receptor molecules on their surface, so there are certainly multiple signaling pathways involved in the development of IPF," Moore says. "But now we know that preventing the binding between the CCL12 ligand and the CCR2 receptor in mice can limit the disease's development."

The CCL12 ligand in mice is virtually identical to the CCL2 ligand in humans, which is known to be involved in other human lung diseases, according to Moore. So antibodies or small molecules capable of blocking CCL2's signal could be promising candidates for new drug discovery.

"We may not be able to stop the initial disease process, but perhaps we could keep it from progressing so rapidly," Moore added. "It's a first step, but an important one, in solving the mystery of this disease. Right now, continued research is the only hope we can offer IPF patients."


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Contact: Sally Pobojewski
pobo@umich.edu
734-615-6912
University of Michigan Health System
23-May-2006


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