Scientists are actively considering the factors that cause autoimmune disorders. They want to understand the immune responses involved.

So far, they have figured that there is PTPN22 which regulates T-cell response. However, the R620W mutation prevents this response from reaching a point where it can interact with other proteins. To investigate the impact of this, researchers have introduced a variant into mice. They have observed increased T-cell activation. Interestingly, T cells carrying the R620W variant in humans displayed the opposite response.

In a recent study, researchers shed light on these conflicting results. They hypothesized that previous human studies with T cells from individuals with autoimmune diseases showed overstimulation and exhausted T cells. To address this, they focused on the naive T cells that had not been exposed to any antigens. By employing a complex editing strategy, they got results that align with previous mouse studies.

This integration provides valuable insights into the function of the R620W variant. Researchers believe that understanding the effects of the observed variant could lead to improved treatments in the future. However, they have cautioned against the practice of inhibiting PTPN22 because it is a negative regulator.