Traumatic brain injury (TBI) afflicts people of all ages, with older adults having the highest rates of TBI-related hospitalizations and deaths among all age groups. Many of the issues and complications that TBI patients face are mediated by the immune response. Aging is a complex process which results in a decline of the immune system due to the altering of cellular production, proliferation and function resulting in an overall decline of immunocompetence. Injury sets off a chain reaction of immune cellular responses, the cell of interest in this project is TH2 cells, which have been shown to play a role in chronic inflammation. The purpose of this study was to explore if the age of an individual influences the TH2 cellular response in relation to traumatic brain injury. The TH2 cells used in the study were collected from younger (aged 21-64) and older (aged 65+) adult participants at < 24hours following mild/moderate TBI and at 3 months post injury. TH2 cells were stimulated with phytohaemagglutinin (PHA) and anti-CD3 and then incubated overnight. They were then analyzed for IL-5 production using the ELISpot assay. The number of cells producing IL-5 were counted, in triplicate, and the mean was taken to determine cellular response when stressed. The results were compared to determine if there is a difference between cytokine release amongst younger and older adults who experience TBI. By having a better understanding of how TH2 cell function is affected by age, we are exploring if overall outcomes following traumatic brain injuries are related to differential immune responses. This knowledge can potentially assist in identifying strategies to improve clinical outcomes.