Platelets, or thrombocytes, are cell fragments in the blood which activate when a person is wounded to induce coagulation. While the role of blood platelets in modulating inflammatory processes is well known, it is less clear their effect on the immune system. Now, Yale Scientists discovered the involvement of platelets in immune response, and found that a protein resulting from platelet activation called Dkk-1 (Dickkopf-Related Protein-1) contributes to chronic inflammation, which plays an important role in autoimmune diseases, asthma, viral infections, and cancer.
Persistent activation of immune cells, in which there is a vicious cycle of tissue destruction and repair, characterizes chronic inflammation. Professor of immunobiology Dr. Alfred Bothwell and his team decided to investigate the role of Dkk-1 in various inflammatory diseases based on previous studies that had already found that Dkk-1 inhibits tissue repair.
The research, published in the Feb. 9 issue of Immunity, showed that inhibiting Dkk-1 genetically or pharmacologically protected mice from house dust mite (HDM)-induced asthma or Leishmania major infection.
“Remarkably, without the presence of Dkk-1, both innate and adaptive immune responses for chronic inflammation could not be triggered,” said Dr. Wook-Jin Chae, associate research scientist from immunobiology and first author. “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.”
“This study could lead to the development of new therapies to treat severe asthma and other inflammatory diseases, the researchers said. The potential in other chronic diseases such as cancer and autoimmunity is enormous,” said Bothwell.
The next step is to harness Dkk-1 in cancer immunotherapy.
“We are looking for small molecule compounds that could block Dkk-1-mediated signaling in the inflamed tissue,” the authors said.
Source: Yale News
