Dr. Peter K. Gregersen, a scientist at North Shore-LIJ’s Feinstein Institute for Medical Research in Manhasset, and his research partners received the royal treatment last week – literally.
Gregersen and his research partners were the recipients of the 2013 Crafoord Prize in Polyarthritis at the Royal Swedish Academy of Sciences in Stockholm, and the person presenting the award was Carl XVI Gustaf, the king of Sweden.
Gregersen and his collaborators, Dr. Lars Klareskog, from the Karoloinska Institute in Stockholm, and Dr. Robert J. Winchester of Columbia University, were being recognized for their work concerning the interactions between genetic and environmental factors and their interactions in the development and management of rheumatoid arthritis, according to a release from the Crafoord Prize’s Web site.
“The knowledge acquired by the 2013 Crafoord Laureates opens new possibilities for the prevention and better treatment of rheumatoid arthritis. Their focused detective work has resulted in a hypothesis that the disease arises from the interplay between genetic inheritance and environmental influences,” the Royal Academy said of Gregersen, Klareskog and Winchester.
Due to their research, a hypothesis has formed that the most common form of rheumatoid arthritis can start in the lungs.
Gregersen, Klareskog and Winchester will share the $600,000 Crafoord Prize, which was established in 1980 by the Royal Swedish Academy of Sciences, which also awards the Nobel Prizes.
“I am honored to receive this prize and proud of the research it celebrates,” Gregersen said in a statement. “Thirty years ago we discovered there is a molecule involved in controlling the immune system and associated with rheumatoid arthritis. More recently it became apparent that this molecule interacts with smoking and leads to an altered immune response present in rheumatoid arthritis – this discovery changed our way of thinking and led to a better understanding of how the rheumatoid arthritis develops.”
Gregersen and his researchers found that smokers carrying a protein called the human leukocyte antigen, which sits on the surface of cells and forms a pocket in which molecules from the cell can get stuck, dramatically increased their risk of developing rheumatoid arthritis.
Immune cells constantly check the contents of such pockets, and if a virus were to infect a cell, parts of the virus would get stuck in the pocket and would then be eliminated by the immune system.
Gregersen, Winchester and Klareskog found that certain variations of the human leukocyte antigen increased the risk for rheumatoid arthritis because their pockets form a special shape.
They also found that smokers would be even more at risk if they also carried antibodies against citrullinated proteins, which increase inflammation and tissue injury.
Because of this research, scientists now believe that citrullinated proteins can fit into the pockets formed by the human leukocyte antigens, and the disease can develop years before awakening.