In the face of an attack or an infection, T cells differentiate form Effector T cells which in turn form Memory T cells like CD4+ T cells that are essential for the formation of protective memory CD8+ T cells following immunization. Cytotoxic CD8+ T cells and helper CD4+ T cells are like special agent twins of our body’s immune system. They are both generated in the thymus and express the T cell receptor.
Consistent with findings through a study carried out by researchers at the University of Helsinki and the Institute for Molecular Medicine Finland, the accumulation of mutations in genes linked with the regulation of immunity and cell proliferation like the ones discussed above could drive rheumatoid arthritis in a similar way to how somatic mutations drive cancer. More specifically, about 30 mutations in CD8+ cytotoxic T cells of 5 out of 25 rheumatoid arthritis patients compared to a single mutation in one out of 20 healthy patients was found.
This phenomenon has been extensively studied in tumors, but this study is the first to investigate it in other diseases.
An important piece of information to note here, although not explicitly put is that all mutations were found in cytotoxic CD8+ T cells, and not a single
During the investigation, another chunk of information that was brought to the fore was that in other 82 rheumatoid arthritis patients, no mutations were found, hence providing evidence as this being driven by the process of accumulation of nonspecific mutations.
“For now, there is no certainty on how these mutations affect the regulation of chronic inflammations. They may be, for lack of a better word, ‘genomic scars’ formed as a result of the activation of the immune defense system. In any case, this research project revealed a new connection on the molecular level between autoimmune diseases and cancer, which brings us one step closer to understanding these diseases.” Says lead scientist of the project, Professor Satu Mustjoki.
