Recent discoveries may help finding a better treatment – and even vaccines – for Lupus
Good news to lupus patients – and people suffering from all autoimmune diseases!
Researchers at St. Jude Children’s Research Hospital identified the series of molecules that guide a sub-set of immune cells, which may be the key for future vaccine improvements and autoimmune therapies.
The immune system uses T cells to kill pathogens – bacteria or viruses – on or inside cells, and B cells to produce antibodies to destroy pathogens circulating in the blood. T follicular helper (TFH) cells are a specialized subset of T cells that help B cells produce antibodies. CXCR5, a protein on the surface of T cells, is necessary for these TFH cells to work correctly. If they don´t, the immune system can attack the own body cells – which could be the case in autoimmune diseases, such as lupus.
Using powerful genetic screening techniques, Hongbo Chi, Ph.D., and colleagues found the key pathway controlling TFH cell development and function, including how TFH cells trigger antibodies.
This intricate discovery has broad significance for therapies that modulate – either strengthen or suppress – the immune system. The discovered pathway may be targeted for therapies to fine-tune TFH cell responses, leading to a well-functioning immune system that is carefully calibrated to attack pathogens while ignoring the body’s own healthy cells.
For example, strengthening this pathway in TFH cells can boost a person’s immune response to a vaccine, making the vaccine more effective. In autoimmune patients, where antibodies attack a person’s own cells, reducing the activity of this specific pathway may decrease harmful antibody production. Further studies are being conducted to explore these possible approaches to new treatments.
“Understanding how TFH cells are regulated opens up doors for new therapies for autoimmune diseases like lupus. When we understand the molecular pathways, we can find particular molecules to target to amplify or suppress the immune system.