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Radiation-induced brain injury (RIBI) is a serious complication of radiotherapy for head and neck tumors, mostly 3-5 years after the end of radiotherapy, clinically manifested as cognitive impairment or epilepsy, pathological changes into brain tissue edema, necrosis, etc.
, seriously affecting the quality of life of patients
。 At present, the pathogenesis of radiation brain injury is unclear and the treatment methods are limited, making the clinical prevention and treatment of radiation brain injury one of
the key problems in the field.
On January 5, 2023, Professor Tang Yamei's team from the Brain Science Research Center of Sun Yat-sen Memorial Hospital of Sun Yat-sen University published a report entitled Microglia drive transient insult-induced brain injury by chemotactic recruitment of CD8 in the journal Neuron + T lymphocytes' research paper elucidates the mechanism by which microglia secrete chemokines CCL2 and CCL8 after radiation attract CD8+ T cells to infiltrate brain tissue and cause brain damage, and propose a new intervention strategy
for the treatment of radiation brain injury.
In recent years, in neurological diseases such as Alzheimer's disease and Parkinson's disease, the infiltration of cerebrospinal fluid and brain tissue, an important participant in acquired immunity, by T lymphocytes, has been successively discovered.
However, the mechanism and possible pathogenesis of T lymphocyte infiltration into the central nervous system remain to be elucidated
.
In this study, in order to systematically study the cell types and molecular mechanisms involved in radiation brain injury, the authors first performed single-cell transcriptome sequencing analysis on tissue samples obtained during resection of radiation brain injury lesions, and found that there was significant CD8+ T cell infiltration in the lesions
.
At the same time, single-cell TCR sequencing results for different patient lesions also showed that CD8+ T cells infiltrating brain tissue underwent significant clonal expansion
.
According to the previous research results of the group (He, et al, FASEB journal, 2020), the authors prepared a radioactive brain injury model in CD8a-DTR transgenic mice and wild-type mice, and systematically knocked out systemic CD8 using diphtheria toxin or Cd8a neutralizing antibody in CD8a-DTR transgenic mice and wild-type mice + T cells, which found that the brain injury lesion was significantly reduced after CD8+ T cell knockout, confirming that CD8+ T cells play a key role
in mediating the occurrence of radiation brain injury.
Next, the authors further explored
the mechanism of how CD8+ T cells infiltrate brain tissue after radiation.
Through cell interaction analysis, it was found that a group of microglia subsets with high expression of chemokines such as CCL2 and CCL8 may trigger the chemotaxis of CD8+ T cells into the brain
.
Using RNAscope staining, in vitro experiments, microglia-specific knockout of CCL2 or CCL8 transgenic mouse models, neutralizing antibodies and small molecule inhibitors, the authors demonstrated that intervention in the CCL2/CCL8-CCR2/CCR5 signaling pathway can effectively inhibit CD8+ T cell migration and significantly reduce the focus
of radiation brain injury.
In other neurological diseases such as cerebral ischemia, there has also been a literature report of infiltration of peripheral CD8+ T cells into the central nervous system
.
Therefore, the research team further explored whether the above CCL2/CCL8-CCR2/CCR5 signaling pathway is also involved in other brain diseases, and finally determined that blocking this signaling pathway can significantly reduce brain damage
caused by middle cerebral artery ischemia (MCAO).
This study is the first to prove that after the brain is stimulated by radiation or cerebral ischemia, microglia secrete chemokines CCL2 and CCL8, attract peripheral CD8+ T cell infiltration, and release cytotoxic factors such as perforin and granzyme, causing secondary damage
to the brain.
At the same time, this paper also provides an innovative theoretical and experimental basis
for the prevention and treatment of brain diseases such as radiation brain injury and cerebral ischemia by inhibiting T lymphocyte-mediated acquired immunity.
Shi Zhongshan and Yu Pei, postdoctoral fellow of the Department of Neurology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Chen Sitai, associate researcher and research assistant of Lin Weijie, are the co-first authors of the paper, and Professor Tang Yamei is the only corresponding author
of the paper.
The research was also supported by Professor Long-Jun Wu of the Mayo Clinic and Professor Ho Ko of the Chinese University of Hong Kong
.
Postdoctoral and full-time researchers recruit
Professor Tang Yamei's research group of the Brain Science Center of Sun Yat-sen Memorial Hospital of Sun Yat-sen University, whose research direction is cerebrovascular disease and the role of neuroimmunity in neurological diseases, and is good at in-depth exploration of pathogenesis and interdisciplinary research
according to clinical phenomena 。 In the past 5 years, as the corresponding author, he has published many high-level academic papers in journals such as J Clin Oncol, Neuron, eClinicalMedicine, Clin Cancer Res, Neurology and so on
.
Due to the needs of research work, we are now recruiting postdoctoral fellows and full-time researchers (including special researchers, special associate researchers and research assistants) in neurobiology, neurology, immunology, bioinformatics and other related majors
.
Job requirements: strong interest in scientific research, active thinking, strong independent work ability and English writing ability, full of team spirit
.
The research group will provide excellent scientific research environment and software and hardware support to promote personal development
in an all-round way.
If you are interested, please scan your resume and 1-2 representative works to send
it by scanning the QR code below.
Resume delivery (interested parties please send personal resume and other materials to): https://jinshuju.
net/f/ZqXwZt or scan the QR code Submit your resume
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