Related Experiment Video
Updated: Jun 24, 2026
Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
[Relationship between cellular immune response and apoptosis of the brain neurons after brain trauma in rats]
Ke-Jia Chen1, Wei Li, Zhi-Gang Wang
1Department of Emergency Medicine, First Affiliated Hospital, Jinan University, Guangzhou, China. tchkejia@126.com
Insights
Brain trauma increases CD4(+) and CD8(+) T lymphocytes, leading to neuronal apoptosis and worsening brain injury. These immune cells peak 10 days post-injury, correlating with neuron death.
Area of Science:
- Neuroscience
- Immunology
- Trauma Research
Context:
- Traumatic brain injury (TBI) is a significant cause of neurological damage.
- The role of the immune system, specifically T lymphocytes, in TBI pathogenesis is not fully understood.
Purpose:
- To investigate the relationship between CD4(+) and CD8(+) T lymphocyte infiltration and neuronal apoptosis in the local traumatic brain tissue following TBI in a rat model.
- To quantify the temporal changes in T lymphocyte populations and neuronal apoptosis post-TBI.
Summary:
- Following TBI in rats, immunohistochemistry revealed a significant influx of CD4(+) and CD8(+) T lymphocytes into the injured brain tissue, peaking around day 10 (15-fold and 20-fold increases, respectively).
- Neuronal apoptosis followed a similar temporal pattern, with a strong positive correlation observed between T lymphocyte numbers and apoptotic neurons.
- Both T lymphocyte counts and neuronal apoptosis began to decline by day 30 post-injury.
Impact:
- TBI triggers a robust cellular immune response involving CD4(+) and CD8(+) T lymphocytes.
- This immune response plays a critical role in mediating neuronal apoptosis, thereby exacerbating secondary brain injury.
- Findings highlight potential therapeutic targets within the adaptive immune system for mitigating TBI-induced damage.
Objective:
To investigate the relation between CD4(+) and CD8(+) T lymphocyte infiltration and apoptosis of the neurons in the local traumatic brain tissue after brain trauma in rats.
Methods:
In rat models of brain trauma, the changes in the number of CD4(+) and CD8(+) T lymphocytes and the apoptosis of neurons in the local traumatic brain tissue were observed by immunohistochemistry at different time points after brain trauma.
Results:
Twenty-four hours after brain trauma, a significant increase in the number of CD4(+) and CD8(+) T lymphocytes occurred in the injured brain tissue, both reaching the highest levels on day 10, at the point of which the number of CD4(+) cells increased by about 15 folds and that of CD8(+) cells by about 20 folds compared with the control groups. The CD4(+) and CD8(+) T lymphocytes both began to decrease 30 days after the injury. A similar pattern of alterations was found in the apoptosis of neurons in the local brain tissue. Correlation analysis demonstrated a close positive correlation between the changes in CD4(+) and CD8(+) lymphocyte numbers and the number apoptotic neurons in the injured brain tissue.
Conclusions:
Brain trauma induces obvious increases in CD4(+) and CD8(+) T lymphocytes and enhanced cellular immune response in the injured brain tissue to mediate neuronal apoptosis and further exacerbate the brain tissue injuries.
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