Study results derived from animal immune system models of rheumatoid arthritis show that deactivating the B-lymphocyte protein PTP1B allows the B-cell to become more responsive.
Deactivating the immune system B-lymphocyte protein PTP1B in animal models allowed the B-cells to become more responsive to activating signals causing rheumatoid arthritis, according to a study published in The Journal of Experimental Medicine.
In a clinical investigation, researchers from the Max Planck Institute of Immunobiology and Epigenetics in Freiburg, Germany learned that patients with rheumatoid arthritis produce unusually low amounts of PTP1B when compared to other cell types and healthy patients. The scientists then used mice, which the team had developed in the ‘90s with the ability to switch off specific genes using Cre-lox genetic engineering technology, to model the absence of the protein.
Deactivating the protein PTP1B allowed the B-cell to become more responsive to activating signals causing rheumatoid arthritis. Similarly, the B-cells also reactivated other cells.
“Mice with a B cell—specific PTP1B deficiency show increased T cell–dependent immune responses and elevated total serum IgG,” the authors write. “Our data suggest that PTP1B plays an important role in the control of B cell activation and the maintenance of immunological tolerance.”
Previously, the B-cells were known as antibody producers, but these results lead scientists to believe PTP1B could have a monitoring function within the cell’s immune response system.