A Montreal Clinical Research Institute team recently published an important study which could bring new therapeutic perspectives in the field of immunology.
Led by Woong-Kyung Suh, director of the IRCM Immune Regulation Research Unit and published in Life Science Alliance, the study brings new light on the critical role of the ICOS protein in the immune response, especially on the development of certain autoimmune diseases.
In fact, people with no ICOS sometimes develop autoimmune symptoms such as rheumatoid arthritis, a disease where the immune system generates antibodies attacking healthy cells in the joints.
What We Know About the Immune System
For decades now, the scientific community has studied the immune system’s central role in protecting the body against threats, thanks to a very complex and integrated network of cells, organs, proteins and tissues. White blood cells (leukocytes) are the immune system agents with the important task to detect and neutralize threats, whether infectious agents such as pathogens and viruses, toxins, or any foreign body considered dangerous. Among white blood cells, lymphocytes play a key role: B cells produce antibodies and T helper cells guide B cells to do so.
Autoimmune reactions happen when the immune system mistakes own body cells for dangerous pathogens. Although the scientific knowledge of the immune systems has increased dramatically in the last decades, many underlying mechanisms are still poorly understood, especially when it comes to what causes faulty autoimmune responses.
New light on the role of ICOS protein
By conducting various experiments in a preclinical model very similar to the human molecular immune system, the team brought to light an underlying mechanism of the production of autoantibodies, the antibodies that attack the body’s own cells thus increasing the chances of developing autoimmune diseases.
Using this model, the team turned off ICOS while stimulating the immune cells by an infection and observed a higher production of autoantibodies in large part due to a decreased number of activated T cells termed “Tfr cells”. Their observations showed that ICOS is necessary for the maturation of precursor T cells into fully functioning Tfr cells. These Tfr cells then suppress B cells that produce disease-related autoantibodies.
“Now that we know that maintaining high levels of fully functioning Tfr cells help control the production of disease-causing autoantibodies, the next step for us is to try finding a drug that could stimulate the production these Tfr cells when the body cannot do it. It is a very possible therapeutic avenue to be explored,” explained Dr. Suh
Acknowledgements
The study was conducted by former PhD student Vincent Panneton (first author), and three current PhD students, Antoine Bouchard, Saba Mohammaei, Nikoletta Diamantopoulos. This research was funded by CIHR (Operating grant) and FRQS (studentship to Vincent Panneton and Antoine Bouchard).
