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B-cells aggravate autoimmune diseases

Scientists in Freiburg may have discovered a fundamental aggravating factor in autoimmune diseases. If B-lymphocytes lack the protein PTP1B, the cells will become hyperactive for stimulatory signals and can thus promote an autoimmune attack. This study offers an additional explanation to how B-cells regulate an immune response.

In Germany, approximately 800,000 people suffer from rheumatoid arthritis. In this progressive disease, a person’s own immune system attacks and destroys connective tissue. However, the most important factors governing the progress of the disease are still unknown. Now, scientists working with Michael Reth and David Medgyesi from the Max Planck Institute of Immunobiology and Epigenetics have identified a factor that may play a significant role. Using genetic engineering, they deactivated the PTP1B protein in B-cells in the immune systems of mice. The B-cells then became much more responsive to activating signals and, in turn, served to reactivate the other cells.

PTP1B could therefore have a monitoring function in the B-cell-mediated immune response. Until now, B-cells were mainly known for producing antibodies after coming into contact with pathogens. Only recently is more and more accepted by researchers that B-lymphocytes possess important regulatory function in the immune system. The current study now provides a new detail of this mechanism.

BIONITY