Researchers at UT Southwestern Medical Centre discovered a protein on T cells that serves as a biological "timekeeper", affecting how the body responds to viral infections throughout the day. UT Southwestern scientists validated the findings, publishing them this week in Science Advances. They may have ramifications for infection treatment, cancer immunotherapy, and understanding the impacts of circadian disturbance. 

The study focused on ADRB2, a protein found on the surface of T cells that binds to adrenaline. Researchers discovered that this mechanism modulates circadian rhythm genes within T cells, influencing how well they generate an antiviral response.

"The adrenaline receptor sets the internal clock of virus-specific T cells, which regulates how well they respond to viral infections at different times of day," said David Farrar, Ph.D., Associate Professor of Immunology and Molecular Biology at UT Southwestern. 

According to co-lead author Drashya Sharma, Ph.D., the discovery fills a gap in decades of research on immunological cycles. "Our findings indicate that ADRB2 is essential for managing the daily rhythms in T cells and also affects how well they can turn into types that fight viruses," the researcher stated. 

A WHO representative, when contacted for comment, stated that the study "adds to the growing body of evidence that timing plays a critical role in immune responses and could inform future vaccine administration strategies." 

The body's internal clock, known as the circadian rhythm, regulates functions such as sleep, hormone secretion, and metabolism. Scientists have previously discovered that vaccines administered in the morning can elicit higher immune responses than those provided in the evening. However, the precise mechanisms controlling immunological rhythms remained unknown. 

In previous work, UT Southwestern researchers discovered that T cells lacking ADRB2 had altered circadian gene activity. In this study, mice that were genetically modified to not have ADRB2 in their T cells showed less growth and weaker development of memory T cells after a viral infection. Memory T cells are critical for long-term immunity and the primary targets of vaccinations. 

At the UT Southwestern laboratory complex in Dallas, researchers alternated between computer screens showing gene-expression graphs and animal testing facilities. In one room, mouse cages were monitored using controlled illumination cycles that mimicked day and night settings. 

Dr Farrar said the next round of research will look into additional chemical signals that alter T cell clocks apart from adrenaline. "Because some circadian clock genes function in the absence of ADRB2, we know there are other mechanisms involved. "Identifying them is critical for understanding how to optimise the timing of immune responses," he explained. 

The WHO spokesman stated that, while further human research is needed, these findings may eventually alter worldwide immunisation schedules and treatment regimens.