Scientists at the University of California San Diego discovered a unique form of cell auto-signaling in T cells. This process boosts the immune system's ability to attack tumors, fueling the development of new anti-tumor therapeutics.
T cells help defend against infections and cancer and are stimulated in lymph organs by antigen-presenting cells (APCs), which present antigens to T cells, activating an immune response. The binding of B7 protein on the surface of APCs with the CD28 receptor on T cells drives the T cell immune response.
Recent work has shown that T cells can produce their own B7 protein or get it from APCs, prompting questions about their behavior. The researchers discovered that T cells could self-activate through a process of puckering their cell membrane inwards, which allowed the B7 protein and the CD28 receptor to bind to each other. This auto-stimulation process boosts T cell function, and researchers have confirmed it slows tumor growth in mouse models of cancer.
According to the team, this system could be used as a cancer biomarker, or T cells could be refueled by providing more sources of B7 in the lymph organs or in the tumor itself. Alternatively, the authors suggest developing a cell therapy to deliver engineered T cells with enhanced auto-signaling capabilities directly to patients.
The researchers also noted that this system could be used as a clinical strategy for treating autoimmune diseases. In patients with autoimmune diseases such as lupus or multiple sclerosis, endocytosis inhibitors could be prescribed to prevent the cell from forming concavities, effectively blocking the B7:CD28 interaction to reduce overactive T cell function.
The discovery of T cells' ability to activate themselves through the B7 protein and the CD28 receptor opens new possibilities for anti-tumor therapies. These findings, published in Immunity, demonstrate that T cells can activate themselves in peripheral tissues, which could assist in developing new anti-tumor therapeutics.