Now, new findings by Yale researchers showed that in systemic autoimmune diseases (such as lupus and rheumatoid arthritis), B cells can be activated even in the absence of T cells — thereby leading to suggested news ways of intervention in tackling the process leading to autoimmune diseases.
Recently this same Yale group along with collaborators at Boston University discovered an unexpected role in autoimmunity of Toll-like receptors, previously thought to be stimulated by molecules expressed on microbial pathogens. Shlomchik and his colleagues showed that they can also recognize and react to “self” molecules, in particular mammalian DNA and RNA. When this occurs, these receptors help activate B cells that make the classical autoantibodies of lupus.
The new Yale study now shows that these signals substitute for T cells in starting the autoimmune process in B cells. The researchers propose that once B cells are activated via Toll-like receptors, they can subsequently recruit T cells and that this can lead to a “vicious cycle” of chronic autoimmune disease in which the two types of cell activate each other.
According to Mark Shlomchik, MD, professor of laboratory medicine and immunobiology at the Yale School of Medicine and senior author of the study:
“The findings were surprising because many scientists believed that B cells remain quiet in autoimmune diseases unless they are stimulated first by T cells.
It became a chicken or egg problem. If cooperation between T and B cells is needed to create an autoimmune disease, who falls off the fence first, and why?”
The findings of the said study may explain why treatments that target T cells fared very poorly while the newer treatments targeted at the B cells are working a lot better.
Here’s a brief explanation how B cells work in the immune system:
B cells react against invading bacteria or viruses by making proteins called antibodies. The antibody made is different for each different bug. The antibody locks onto the surface of the invading bacteria or virus. The invader is then marked with the antibody so that the body knows it is dangerous and it can be killed off.
The B cells are part of the memory of the immune system. The next time the same bug tries to invade, the B cells that make the right antibody are ready for it. They are able to make their antibody more quickly than the first time the bug invaded.
What happens here is that, the treatments to work should be able to intervene in the immune system’s attack to the body’s own tissue.
Read more details from Medical News Today.