Scientists at the Helmholtz Centre for Infection Research (HZI) said Friday that too much of a protein called c-FLIPR can trigger autoimmune diseases.
According to the scientists, the protein plays a key role in controlling an "apoptosis" process, also called "cellular suicide" and is crucial for the survival of the body.
Scientists described the significance of c-FLIPR for the immune system in more detail.
"C-FLIPR is important for the balance of the immune system. It might be possible to intervene with suitable therapeutic agents if the equilibrium of the immune system is disrupted," said HZI scientist Ingo Schmitz.
The researchers took a closer look at the exact function of a certain variant of the protein, called c-FLIPR by using mice to investigate what happens if this protein is always present in lymphocytes, a type of immune cells, and other blood cells.
Whereas the apoptosis inhibitor caused no anomalies in young mice, the scenario in older mice was quite different. Scientists pointed out that the inhibitory effect of c-FLIPR on apoptosis is the underlying cause of both these effects.
"The composition of the lymphocytes was changed significantly," said Schmitz, "Furthermore, the immune cells were strongly activated."
The researchers also found immune molecules, called autoantibodies, which attack the body's own tissue in the kidneys and lung and detected harmful protein deposits in the kidneys.
The changes in the lung tissue are also indicative of the immune system attacking its own body in the presence of too much c-FLIPR. Physicians usually see these symptoms in a human autoimmune disease called systemic lupus erythematosus.
HZI said that the scientists discovered last year that cells can fight bacterial infections better if c-FLIPR is turned on permanently. This means that inhibiting the suicide of cells has beneficial effects in acute infections, but leads to autoimmune reactions in the long run.