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Click on the blue letters to pay attention to our innate and adaptive immune cells are activated after cerebral ischemia, and play a key role in debris removal and inflammation subsidence
.
However, excessive or indiscriminate immune activation can cause secondary damage and hinder the repair process of the injured brain
.
Regulatory T cells (T-reg) are mainly composed of a group of CD4+ T cells expressing CD25, Foxp3 and Helios proteins, which play the role of reducing excessive immune response and maintaining immune homeostasis
.
Studies have shown that the number of infiltrating Treg cells in the brain increases after ischemic stroke and continues to increase for at least 1 month after the stroke
.
Treg cells are believed to promote functional recovery after stroke by inhibiting the proliferation of astrocytes
.
Depletion of Treg cells 4 days after stroke inhibits the proliferation of neural stem cells
.
On June 13, 2021, the Xiaoming Hu research team at the University of Pittsburgh School of Medicine published an article in Immunity, revealing that osteopontin derived from Treg cells regulates the tissue repair function of microglia after stroke and exerts a neuroprotective effect
.
Researchers performed single-cell omics sequencing on mouse brains in the subacute phase (significant inflammation and a large number of immune cell infiltrations) and recovery phase (14 days after stroke) after stroke.
The results found that there were 14 types in the subacute phase.
The differentially expressed cell subsets are mainly microglia, neutrophils and specific macrophages; the 11 types of differentially expressed cell subsets during the recovery period are mainly adaptive immune cells
.
After stroke, the number of Treg cells maintains a long-term upward trend.
Further flow cytometry is used to detect Treg cells in the acute, subacute, and chronic phases of stroke.
The infiltrating Treg cells increase significantly from 7 days and last at least 35 days.
.
What is the significance of the long-term existence of these Treg cells? The researchers knocked out these immune cells before the stroke, and the mice's motor dysfunction worsened
.
This indicates that such cells may be beneficial for the repair of brain damage
.
However, knocking out Treg cells did not affect the number of neurons, but the myelin coverage in mice after stroke was significantly reduced
.
Transplantation of Treg cells from normal mice to knockout Treg cells increases myelin coverage, which indicates that Treg cells have little effect on the gray matter of the brain and a great impact on white matter
.
Transmission electron microscopy experiments showed that the thickness of myelin sheath in the brain was significantly reduced after a stroke, but knocking out Treg cells made this worse situation worse, and the thickness of myelin sheath became thinner
.
Oligodendrocytes are the main source of myelin.
They found that knocking out Treg cells reduces the number of new oligodendrocytes in the striatum and transplantation of Treg cells can effectively inhibit the reduction of oligodendrocytes
.
These Treg cells that enter the brain after stroke are enriched and express genes with immune regulation and cell-cell interaction functions, especially the activation signal pathway of phagocytes
.
Morphological analysis found that after knocking out Treg cells, the volume of microglia decreased and the surface area also decreased
.
In vitro cell experiments further confirmed that activated Treg cells can promote the transition of microglia to an anti-inflammatory state, and can promote the further differentiation of immature oligodendrocytes into mature oligodendrocytes
.
Transcriptomics analysis revealed that osteopontin secreted by Treg cells promotes the tissue repair function of microglia through integrin receptors
.
Intraperitoneal injection of IL-2:IL-2Ab antibody to relieve stroke dyskinesia.
Researchers injected IL-2:IL-2Ab antibody (which can increase Treg cells in the periphery and brain) into the abdominal cavity of stroke model mice to promote the repair of myelin sheath , And can significantly improve motor function and cognitive dysfunction
.
In general, this paper found that Treg cells that exist for a long time after stroke and increase in number play a neuroprotective effect by promoting the tissue repair function of microglia
.
[References] 1.
Shi et al.
, Treg cell-derived osteopontin promotes microglia-mediated white matter repair after ischemic stroke, https://doi.
org/10.
1016/j.
immuni.
2021.
04.
022 The pictures in the article are all from the references Original download link: Baidu Netdisk https://pan.
baidu.
com/s/1ypiCikS0TDR4jcqBLDwyaw Extraction code: q4j5
.
However, excessive or indiscriminate immune activation can cause secondary damage and hinder the repair process of the injured brain
.
Regulatory T cells (T-reg) are mainly composed of a group of CD4+ T cells expressing CD25, Foxp3 and Helios proteins, which play the role of reducing excessive immune response and maintaining immune homeostasis
.
Studies have shown that the number of infiltrating Treg cells in the brain increases after ischemic stroke and continues to increase for at least 1 month after the stroke
.
Treg cells are believed to promote functional recovery after stroke by inhibiting the proliferation of astrocytes
.
Depletion of Treg cells 4 days after stroke inhibits the proliferation of neural stem cells
.
On June 13, 2021, the Xiaoming Hu research team at the University of Pittsburgh School of Medicine published an article in Immunity, revealing that osteopontin derived from Treg cells regulates the tissue repair function of microglia after stroke and exerts a neuroprotective effect
.
Researchers performed single-cell omics sequencing on mouse brains in the subacute phase (significant inflammation and a large number of immune cell infiltrations) and recovery phase (14 days after stroke) after stroke.
The results found that there were 14 types in the subacute phase.
The differentially expressed cell subsets are mainly microglia, neutrophils and specific macrophages; the 11 types of differentially expressed cell subsets during the recovery period are mainly adaptive immune cells
.
After stroke, the number of Treg cells maintains a long-term upward trend.
Further flow cytometry is used to detect Treg cells in the acute, subacute, and chronic phases of stroke.
The infiltrating Treg cells increase significantly from 7 days and last at least 35 days.
.
What is the significance of the long-term existence of these Treg cells? The researchers knocked out these immune cells before the stroke, and the mice's motor dysfunction worsened
.
This indicates that such cells may be beneficial for the repair of brain damage
.
However, knocking out Treg cells did not affect the number of neurons, but the myelin coverage in mice after stroke was significantly reduced
.
Transplantation of Treg cells from normal mice to knockout Treg cells increases myelin coverage, which indicates that Treg cells have little effect on the gray matter of the brain and a great impact on white matter
.
Transmission electron microscopy experiments showed that the thickness of myelin sheath in the brain was significantly reduced after a stroke, but knocking out Treg cells made this worse situation worse, and the thickness of myelin sheath became thinner
.
Oligodendrocytes are the main source of myelin.
They found that knocking out Treg cells reduces the number of new oligodendrocytes in the striatum and transplantation of Treg cells can effectively inhibit the reduction of oligodendrocytes
.
These Treg cells that enter the brain after stroke are enriched and express genes with immune regulation and cell-cell interaction functions, especially the activation signal pathway of phagocytes
.
Morphological analysis found that after knocking out Treg cells, the volume of microglia decreased and the surface area also decreased
.
In vitro cell experiments further confirmed that activated Treg cells can promote the transition of microglia to an anti-inflammatory state, and can promote the further differentiation of immature oligodendrocytes into mature oligodendrocytes
.
Transcriptomics analysis revealed that osteopontin secreted by Treg cells promotes the tissue repair function of microglia through integrin receptors
.
Intraperitoneal injection of IL-2:IL-2Ab antibody to relieve stroke dyskinesia.
Researchers injected IL-2:IL-2Ab antibody (which can increase Treg cells in the periphery and brain) into the abdominal cavity of stroke model mice to promote the repair of myelin sheath , And can significantly improve motor function and cognitive dysfunction
.
In general, this paper found that Treg cells that exist for a long time after stroke and increase in number play a neuroprotective effect by promoting the tissue repair function of microglia
.
[References] 1.
Shi et al.
, Treg cell-derived osteopontin promotes microglia-mediated white matter repair after ischemic stroke, https://doi.
org/10.
1016/j.
immuni.
2021.
04.
022 The pictures in the article are all from the references Original download link: Baidu Netdisk https://pan.
baidu.
com/s/1ypiCikS0TDR4jcqBLDwyaw Extraction code: q4j5
