This past week a new study was published that may turn conventional thinking about RA on its ear. Right now, it’s assumed that RA is caused when the body attacks its own healthy cells. This new research has found that there is actually a “target” attached to the cells that are attacked. I’ve put a link to the article at the bottom if you want to read the entire thing.
Researchers at Osaka University have found that people who are susceptible to RA contracted the disease when certain “misfolded proteins” attach to healthy cells rather than being processed into peptides. In healthy people, the proteins are processed normally.
This misfolded protein makes the cell look like an abnormal cell that needs to be destroyed, so the body attacks it. They looked at the disease down to a molecular level and found that molecules that are supposed to bind to part of the abnormal cell targets in order to have lymphocytes recognize the targets for attacks, actually bound to the abnormal proteins. Because of this target attached to an otherwise healthy cell, the lymphocytes attacked the molecules.
In the diagram above, on the left side shows the current thinking where the lymphocyte itself goes abnormal and attacks the healthy cell. The new thinking is the lymphocyte is normal, but it sees a “target” caused by abnormal protein attached to an otherwise healthy cell.
The goal is to develop a drug that is targeted at denatured proteins to
dissolve them, or a method of examination that will allow doctors to make a
diagnosis of the disease at an extremely early stage.
There are some usual “reporter” issues with the article in that they describe RA as resulting in the “slow deterioration of the joints of the hands and feet of patients,” but I put this down as a reporter research problem, not an issue with the study.
All I can say is that I love it when studies such as these open up new avenues of hope for a cure or better detection and treatment options.
I hope whatever treatment option you have is working well. Below is the link to the article.