How does the immune system manage to fight invasive pathogens without damaging the body? And why does it sometimes turn against the body after all? A team from the Chair of Genetics at FAU has been exploring these questions together with the university hospitals in Erlangen and Regensburg.
Certain viral and bacterial infections can trigger autoimmune diseases, for example the borrelia bacteria which can cause Lymes disease after a tick bite. If the infection is not treated, it can lead to inflammation of the joints or the heart months or even years later. One possible explanation for these long-term effects is that the human immune system does not manage to restrict the immune response to the pathogen, and starts to attack the body's own tissue as well.
The FAU team of researchers has now confirmed this hypothesis. It has proven for the first time that a regulatory protein on B cells, a type of white blood cell, has a key role to play. This protein, the inhibitory Fcg receptor IIb, controls the quality and quantity of the protective antibody response. If the receptor does not work correctly, the B-cells, which usually produce protective antibodies, then also produce autoantibodies which attack the body's own proteins, thereby causing inflammation in the tissue and triggering autoimmune disease.
'Our findings indicate very clearly how even slight deviations from the complex regulatory mechanisms of the immune response can lead to significant collateral damage,' explains Prof. Dr. Falk Nimmerjahn, Chair of Genetics.
The results of the study, which contribute to a greater general understanding of immune responses in the context of infections and vaccines, have been published in the journal ELIFE.
