Researchers have discovered that the platelet-derived protein Dickkopf-1 contributes to chronic inflammation, which may represent a new target for conditions such as asthma.

In order to investigate the possible pathological role of Dkk-1 protein in inflammation, the research team, led by researchers at Yale University School of Medicine, studied the effect of a parasite and a common house-dust mite, a common cause for asthma, in normal mice and mice lacking the Dkk-1 protein.

Results showed that blocking Dkk-1 expression, either by genetic or pharmacological manipulation, protected the mice against asthma and parasitic infection. The researchers also observed that the protein induced the polarization of immune T cells towards an inflammatory phenotype, and that Dkk-1 provided a link between platelets, its major source during pathological inflammation, and lymphocytes (important white blood cells). Without Dkk-1, the innate and adaptive immune responses linked to chronic inflammation could not be triggered.

The study results also highlighted the importance of platelets in the immune system and tissue repair in response to inflammation. “Remarkably, without the presence of Dkk-1, both innate and adaptive immune responses for chronic inflammation could not be triggered,” first author Wook-Jin Chae said in a press release. “Because Dkk-1 is from platelets and it inhibits tissue repair, now we know how platelets become an essential part of the immune response and tissue repair simultaneously in response to inflammation.”

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