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Protein that inhibits the development of autoimmune diseases discovered

Scientists have identified the elementary function of the protein, Caveolin-1 in the plasma membrane of B-cells, which prevents the development of autoimmune conditions.

B-cells, the immune system cells that produce antibodies, recognise substances via B-cell antigen receptors (BCR). These protrude from the surface of the cell and, like a type of antenna, ensure that the B-cells recognise all sorts of intruders, such as bacteria or viruses. Once the intruder has been bound by the BCR, the B-cell is activated and, together with other immune cells, can fight off a range of different types of pathogens.

The immune system protects humans from threats, such as disease-causing bacteria and cancer to name a few. Yet if the system malfunctions, it can attack the body it is supposed to defend and cause autoimmune diseases such as type one diabetes mellitus, or multiple sclerosis (MS).

Dr. Susana Minguet, a Biochemist, working in cooperation with Prof. Dr. Michael Reth, the Chairman of the Department of Molecular Immunology at the University of Freiburg, and Prof. Dr. Miguel Ángel del Pozo of the National Center for Cardiovascular Research Carlos III in Madrid, has demonstrated, in a study, that the membrane protein Caveolin-1 plays a key role in immune responses that trigger this type of condition.

Up to now research has often viewed autoimmune disease as the result of immune system hyperactivity, yet recently it has become increasingly clear that such ailments may also result from an immune system where responses are too weak. This finding, which is supported by the researchers' study, could result in new approaches to treating these conditions. Therapies have until recently been aimed at suppressing patients' immune responses. Now, autoimmune conditions could be treated using alternative strategies, such as gene therapy, for example.

Current studies, such as those of Michael Reth, indicate that these antennas are not randomly distributed over the surface of the cell. Instead, they are bundled together in organised protein islands that coalesce as soon as a foreign substance is bound to a B-cell receptor. Minguet and her team have discovered that the protein Caveolin-1 regulates this organisation, making it the key to activation of the B-cells and the triggering of an immune response. Without Caveolin-1, the binding of viruses or bacteria to the B-cell results in a reduced activation signal, which leads to a weakened immune response.

In the body, developing B-cells are educated to distinguish the body's own substances from foreign ones. This process is based on the efficient signal transfer of the B-cell receptors. B-cells that do not produce Caveolin-1 cannot properly organise the receptor on the cell membrane and as a result, efficient signal transfer fails. It is then that B-cells emerge that recognise the body's own tissues. Yet they classify them as foreign, which leads to activation of the B-cell and an undesirable immune response which can result in triggering autoimmune disease. The researchers demonstrated this by conducting experiments on mice.

The team's results have the potential to improve the current understanding of autoimmune conditions and their treatments because up to now, science has lacked suitable animal models that present the same immune deficiencies that are observed in humans.

This study, “Caveolin-1-dependent nanoscale organization of the BCR regulates B- cell tolerance”, was published in the Nature Immunology journal.

Date: 17/08/17

Source: MS-UK

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