When the body hosts invading foreign-bodies that can harm it, certain properties within the immune system are activated so the bodies are analysed and presented to T cells for risk-assessment. This leads to the production of anti-inflammatory regulatory cells and pro-inflammatory T cells that work together to prevent harm to the body.
In recent tests, mice were used to assess how T cells are affected by the size of atherosclerotic lesions, and a new mechanism was identified that directly links regulatory T cell activation with protection from atherosclerosis. The mice used in the research, possessed cells which lacked MYD88-protein that helps cells to develop and mature so they are able to function correctly. As undeveloped cells cannot activate T cells – the absence of MYD88 halted the production of both effector and regulatory T cells – leaving mice prone to the development of atherosclerosis.
Previous studies had suggested that the opposite would happen, according to Dr Tabas at the CUMC:
“In those studies, researchers disabled cells at an earlier stage, creating all sorts of compensatory processes,” said Dr. Tabas. “That’s probably why they came to a different conclusion. In our model, we were able to knock out only the step involved in activating T cells, leaving everything else alone.”
These findings can help produce vaccines that are more effective and foster a greater understanding of how T cells operate within the body.