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Taken together, these observations demonstrate that immune surveillance of the CNS is ensured by allowing activated immune cells access via the BBB and the BCSFB to the CSF space, where they can interact with the antigen presenting cells.
The diffusivity of TCR is similar in T cells at different stages of activation, indicating that this parameter is not involved in allowing activated T cells to be more responsive to antigenic stimulation.
These results show that the basic parameters of TCR dynamics on the surface of T cells are not significantly different in T cells at different stages of activation, indicating that TCR mobility is not involved in allowing activated T cells to be more responsive to antigenic stimulation.
Structural analyses revealed that in contrast to the compact conformation of the dimeric YfiB alone, YfiBL43P adopts a stretched conformation allowing activated YfiB to penetrate the peptidoglycan (PG) layer and access YfiR.
11 These bound T cells secrete matrix metalloproteinases (MMPs) that compromise the extracellular matrix proteins of the subendothelial basement membrane of the blood brain barrier, thereby allowing activated macrophages to enter the CNS and demyelinate axons.
MMPs participate in angiogenesis by degrading and remodelling the extracellular matrix and basement membranes, allowing activated endothelial cells to proliferate and migrate, as well as releasing extracellular matrix-bound growth factors such as FGF-2, VEGF or IGF-1 [ 36].
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The expression of this receptor is markedly upregulated upon T-cell activation, which allows activated T cells to migrate towards sites of inflammation.
At least two nucleation mechanisms allow explaining the experimental results: the introduction of seeds causes a significant burst of surface nucleation and the continuation of the cooling process, through the generation of continuous supersaturation, allows activated secondary nucleation to take place.
BIS-1 allows activated T cells to specifically recognise and kill EGP-2-positive but not EGP-2-negative target cells.
A new treatment is being introduced in the form of a bispecific antibody (Emicizumab) targeted to both FIXa and FX, and which allows activating FX by FIXa without the need for FVIII.
TMS/EEG allows activating directly a subset of cortical neurons and recording the immediate effects of this initial activation in the rest of the brain.
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