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Posted On: 07/08/2025 5:50:34 PM
Post# of 155051
Yes the following is AI generated, but sounds like what we all think:
1. Relevance of CCR5 in Neuroplasticity and Ischemic Stroke (IS)
The study identified CCR5 and CXCR4 among five hub genes involved in neuroplasticity after IS.
CCR5 was specifically expressed in microglia and macrophages, key players in the neuroinflammatory response post-stroke.
CCR5 was positively associated with activated dendritic cells (aDCs) and T helper cells, suggesting a regulatory role in post-ischemic immune responses and potential influence on the inflammatory environment that affects neuronal recovery and plasticity.
2. Leronlimab’s Mechanism of Action and Implication for IS Therapy
Leronlimab blocks CCR5, thereby interfering with the CCR5/CCL5 signaling axis.
This blockade:
Reduces inflammatory chemotaxis of immune cells such as T cells and macrophages to injury sites.
May modulate the immune response post-stroke, thereby reducing secondary damage due to neuroinflammation.
Could promote neuronal recovery and synaptic remodeling by altering the immune microenvironment, enhancing neuroplasticity.
This aligns with emerging evidence that CCR5 inhibition can promote recovery after central nervous system injury, including stroke. Notably, a 2016 Cell study (Joy et al.) showed that CCR5 knockout in mice led to enhanced recovery post-stroke due to increased cortical plasticity and axonal sprouting.
3. Integration with Study’s Methodology and Findings
Bioinformatics and single-cell analysis showed:
CCR5 expression in microglia/macrophages supports the idea that it plays a role in regulating the innate immune environment after IS.
The positive association of CCR5 with T helper cells and aDCs suggests that Leronlimab may downregulate pro-inflammatory signaling that hinders neuronal repair.
DGIdb database predictions identified Leronlimab as a promising CCR5-targeting molecule, validating its inclusion as a candidate therapeutic.
4. Summary Application of Leronlimab to the Study
Leronlimab’s selective antagonism of CCR5 directly addresses a core pathway implicated in the study: the modulation of immune-driven neuroplasticity post-ischemic stroke. By targeting CCR5:
It may reduce maladaptive neuroinflammation, particularly in microglial/macrophage populations.
It could enhance neural repair mechanisms by altering T-cell and dendritic cell activity in the ischemic environment.
It stands as a biologically plausible intervention for improving functional outcomes in IS patients by fostering a more regenerative cellular microenvironment.
1. Relevance of CCR5 in Neuroplasticity and Ischemic Stroke (IS)
The study identified CCR5 and CXCR4 among five hub genes involved in neuroplasticity after IS.
CCR5 was specifically expressed in microglia and macrophages, key players in the neuroinflammatory response post-stroke.
CCR5 was positively associated with activated dendritic cells (aDCs) and T helper cells, suggesting a regulatory role in post-ischemic immune responses and potential influence on the inflammatory environment that affects neuronal recovery and plasticity.
2. Leronlimab’s Mechanism of Action and Implication for IS Therapy
Leronlimab blocks CCR5, thereby interfering with the CCR5/CCL5 signaling axis.
This blockade:
Reduces inflammatory chemotaxis of immune cells such as T cells and macrophages to injury sites.
May modulate the immune response post-stroke, thereby reducing secondary damage due to neuroinflammation.
Could promote neuronal recovery and synaptic remodeling by altering the immune microenvironment, enhancing neuroplasticity.
This aligns with emerging evidence that CCR5 inhibition can promote recovery after central nervous system injury, including stroke. Notably, a 2016 Cell study (Joy et al.) showed that CCR5 knockout in mice led to enhanced recovery post-stroke due to increased cortical plasticity and axonal sprouting.
3. Integration with Study’s Methodology and Findings
Bioinformatics and single-cell analysis showed:
CCR5 expression in microglia/macrophages supports the idea that it plays a role in regulating the innate immune environment after IS.
The positive association of CCR5 with T helper cells and aDCs suggests that Leronlimab may downregulate pro-inflammatory signaling that hinders neuronal repair.
DGIdb database predictions identified Leronlimab as a promising CCR5-targeting molecule, validating its inclusion as a candidate therapeutic.
4. Summary Application of Leronlimab to the Study
Leronlimab’s selective antagonism of CCR5 directly addresses a core pathway implicated in the study: the modulation of immune-driven neuroplasticity post-ischemic stroke. By targeting CCR5:
It may reduce maladaptive neuroinflammation, particularly in microglial/macrophage populations.
It could enhance neural repair mechanisms by altering T-cell and dendritic cell activity in the ischemic environment.
It stands as a biologically plausible intervention for improving functional outcomes in IS patients by fostering a more regenerative cellular microenvironment.
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LETS GO!!!
