23 January, Washington D.C
US researchers have identified a molecule required for immune cells to enter the joints that could lead to new treatment approaches for inflammatory arthritis.
Researchers of the Massachusetts General Hospital (MGH) have found that that tracking immune cells can assist in identification of inflammatory arthritis.
The findings indicate that specific molecule – complement C5a – is required to cause the immune cells called neutrophils to adhere to joint surfaces and migrate into the joint, a process known to set off the inflammatory cascade.
The study, published in the journal of Science Immunology, has identified the initial steps leading to joint inflammation in a model of inflammatory arthritis.
“Inflammatory arthritis is caused when immune cells are recruited from the blood into the joint in a highly regulated process controlled by chemoattractants and adhesion receptors,” said senior author Andrew Luster.
“But when the disease has become symptomatic, it is difficult to determine the initial steps that set off the recruitment of immune cells into the joint and the specific roles of the different chemoattractants,” Luster added.
To better determine the role of specific chemoattractants in type III hypersensitivity, lead author Yoshishige Miyabe, used multiphoton intravital microscopy – an imaging technology for studying immune cell movements in living animals.
The results revealed that the presence of ICs within the joint space induces the generation of complement C5a, a component of the innate immune system, which is then displayed on the inner walls of adjacent blood vessels.
C5a directly initiates the adherence of neutrophils to the vessel walls through interaction with the C5a receptor on neutrophils, which then pass into the joint space and set off the inflammation.
“The control of immune cell entry into the joint represents a major point at which new therapies could be developed to reduce the symptoms of inflammatory arthritis,” Luster stated.