Type 1 diabetes (T1D) is a major childhood autoimmune disease that results from the destruction of insulin-producing beta cells by islet-reactive T cells, making patients on dependent on insulin replacement for survival. However, insulin replacement is not a cure and many patients suffer long term complications, including cardiovascular, renal and neuropathy. We hypothesize that lack of therapy to protect at risk individuals or slowing loss of beta cells in newly diagnosed patients are a result of lack of key information regarding how the disease develop.
I am doing my research at Hamad’s lab in the department of Pathology. We have discovered a new adaptive immune cell that combines lineage characteristics of both B and T cells and clonally expanded in Type 1 Diabetes patients. We refer to this hybrid lymphocytes as dual expressers (DEs) because they co-express the B cell receptor (BCR) and the T cell receptor (TCR) and we generally call them “X cells” to denote their crossover phenotype. Phenotypic and functional characteristics of X cells which are recently published in the prestigious Journal Cell are expected to open a new line of research that can lead to new breakthroughs in the field of autoimmunity that are relevant not only to type 1 diabetes but also are other autoimmune diseases such as multiple sclerosis, lupus.
Briefly, our findings indicate that the X cell are major drivers of type 1 diabetes by bearing an insulin mimic that cross-stimulates insulin-reactive T cells that go on to infiltrate pancreas and destroy insulin-producing beta cells. We believe these findings together with our ongoing research are preparing the platform for developing a biomarker that helps screen individuals at risk for developing Type 1 diabetes at very early age, possibly at birth and lay the groundwork for developing immunotherapies that target X cells for elimination for protecting at risk individuals.