Novel role of mitochondria in immune function

Novel role of mitochondria in immune function

Previous studies have shown RIPK3 controls the induction of a type of programmed cell death, called necroptosis, which protects the body from harmful mutations and infections. However, scientists had not fully understood RIPK3's role in the immune system. 

In the study published in nature Communications, scientists show that RIPK3, relays signals between the cell's mitochondria "powerhouses" and the immune system.
The new study also shows that this crosstalk is important not only for launching immune responses against tumors, but also for regulating the inflammatory responses that may result in autoimmune diseases.

Research suggests that RIPK3 regulates the activation of natural killer T cells (NKTs), the immune cells that play dual roles in the development of autoimmune diseases and the destruction of cancers. RIPK3 doesn't directly cause necroptosis; instead, it regulates the activity of a mitochondrial enzyme (PGAM5) to trigger the expression of inflammatory cytokines in NKTs.

The new study also suggests there may be a way to intervene in the pathway to block inflammation. When the researchers deleted the gene for RIPK3 or inhibited other parts of the pathway, they found they could actually protect mice from the induction of acute liver damage, implying a role for RIPK3 in autoimmune diseases.