Protein Found to Play Key Role in Triggering Autoimmune Diseases
Study findings may improve treatment options for autoimmune disease.
Scientists have identified a membrane protein that inhibits the development of autoimmune diseases.
It was commonly believed that autoimmune disease is the result of immune system hyperactivity, but new findings suggest it may also result from an immune system with too weak of a response.
In a study published in Nature Immunology, investigators identified the elementary function of Caveolin-1 (Cav1) in the plasma membrane of B cells, which produces antibodies.
B cells recognize substance via B cell antigen receptors (BCR), which protrude from the surface of the cell to ensure the B cells recognize intruder bacteria or viruses. Once the intruder is bound by the BCR, the B cell is activated and fights off different types of pathogens with other immune cells.
Recent studies indicate the protrusions or antennas are not randomly distributed across the cell’s surface, but rather are grouped together in organized protein bundles that coalesce as soon as the invader is bound to a B cell receptor.
In the current study, investigators found that Cav1 regulates this organization playing a role in the key activation of the B cells and triggering an immune response. When Cav1 is absent, viruses or bacteria that bind to the B cell produces a reduced activation signal, which leads to a weakened immune response.
Developing B cells can distinguish between the body’s own substances and foreign ones via the efficient signal transfer of the B cell receptors. When B cells fail to produce, Cav1 cannot properly organize the receptor on the cell membrane, causing the signal transfer to fail, according to the study.
Unfortunately, when B cells emerge, they begin classifying the body’s own tissues as foreign. This leads to activation of the B cell and an immune response that can result in triggering autoimmune disease, according to the study.
The findings have the potential to develop and improve treatment options for autoimmune diseases, the authors concluded.