Scientists at UCLA’s Jules Stein Eye Institute and Harbor-UCLA Medical Center discovered defects in the infection-fighting T-cells of GD patients?immune systems. Reported March 1 in the Journal of Immunology, their study may deepen understanding of how the autoimmune disorder damages the body and offer a new target for treating the disfiguring disease.
Earlier research found that GD patients?immune systems produce an antibody that other people do not. Not recognizing the patient’s thyroid as "self," the antibody mistakenly mounts an attack against the organ, causing inflammation and damage to the body, including eye tissue.
In the current study, UCLA researchers discovered that T-cells taken from GD patients contain an abnormal surplus of the receptor targeted by this antibody. An antibody must latch to a specific receptor ?like a key into a lock -- in order to elicit a cellular response. The receptors mobbed the patients?immune systems, even on T-cells that normally would not produce them.
"We didn’t know why GD patients?cells created a new antibody, but had a hunch that that it sprang from an immune abnormality," explained Dr. Raymond Douglas, first author and assistant professor of ophthalmology at the Jules Stein Eye Institute. "Because T-cells are the generals of the immune system and lead the attack in any immune response, we assumed that they played a key role in this antibody’s development."
The team tested GD patients?blood for the antibody and compared their findings to samples from healthy people, with about 100 subjects in each group. The new antibody was found in almost all of the GD patients?blood.
The new antibody binds to the excess receptors on the T-cells, mimic
Source:University of California - Los Angeles