Scientists at The Scripps Research Institute have discovered a critical role played by an enzyme in cancer and autoimmune diseases. Their findings could help in the development of therapy for the diseases.
The scientists have found that the enzyme receptor-interacting serine-threonine kinase-3 (RIPK3) has a role not previously known: sending messages between the mitochondria "powerhouses" of the cells and the immune system, according to an article published in the journal Nature Communications and reported by Yvette Brazier in Medical News Today.
According to the research, the communication performed by RIPK3 has two roles: first, to launch immune responses against tumors, and second, to regulate inflammatory responses that may result in autoimmune diseases. Scientists already knew that RIPK3 controlled the induction of necroptosis, a type of programmed cell death. While necroptosis protects the body from harmful mutations and infections, its role in the immune system is only now becoming understood.
In order to gain a better understanding of RIPK3, the Scripps researchers studied RIPK3-deficient mice. They determined that RIPK3 seems to regulate the activation of natural killer T cells (NKTs). These NKTs are immune cells that have a function in both the development of autoimmune diseases and the destruction of cancer.
Researchers believe that RIPK3 regulates the activity of a mitochondrial enzyme known as PGAM5, and this, in turn, initiates the expression of inflammatory cytokines in NKTs. The scientists now hope that understanding this pathway will help to achieve better ways to control NKTs in order to attack tumors. They also think that understanding the pathway can also make it possible to disrupt it in order to block inflammation. When the researchers detected the gene for RIPK3, or blocked other parts of the pathway, they discovered that they could actually protect mice from acute liver damage. They believe that this might mean that there is a role for RIPK3 in autoimmune diseases.
According to the Scripps Research Institute (TSRI) Assistant Professor of Immunology Young Jun Kang, who collaborated on the study with the lab of TSRI Institute Professor Richard A. Lerner -- who is also Lita Annenberg Hazen Professor of Immunochemistry, "This finding could be helpful for developing strategies to target cancer and inflammatory diseases."
The next step will be to focus on understanding the details of this new signaling pathway. Once the scientists have reached that stage, they think the research will pave the way for new therapies to either enhance its cancer-killing role or reduce its role in inflammation.