Traumatic brain injury (TBI) is considered a major epidemiological and socioeconomic issue of the modern age, due to traffic accidents, sports, or warfare injuries. Although there are several established animal models of TBI that portray different patterns of injury caused by brain trauma and that shed light upon pathophysiological sequelae, much is still unknown about the link between immune response and TBI. The aim of this research was to investigate the infiltration of T cells, indicating activation of the adaptive immunity in the brain tissue, within the first week after experimental TBI in the rat. Lateral fluid percussion injury (LFPI), a model of TBI causing both focal cortical lesion and diffuse damage in the ipsilateral hemisphere, was induced in male Wistar rats. Experiments were divided into two parts. One experiment was conducted to evaluate the time course of neuroimmune mechanisms, with animals being sacrificed at 1, 3, or 7 days post-TBI. The other arm consisted of the application of the enoxaparin (1 mg/kg), low molecular weight heparin to the rats exposed to LFPI. After the injury, animals were administered with vehicle or enoxaparin over the course of 48 hours. Sham craniotomy and vehicle treatment were performed on the control group. The results of this study show the invasion of CD3+, CD4+, and CD8+ cells in the cortices of the brain-injured animals. Enoxaparin treatment did not affect CD3+ or CD4+ cell numbers in the cortices of injured animals as it also had no significant effect on the TBI-induced neuromotor impairment. In conclusion, the results of this study indicate that the LFPI model of TBI can elicit a cellular immune response, although significant effects of enoxaparin were not observed.