Deans' stroke musings: Brain regulatory T cells suppress astrogliosis and potentiate neurological recovery

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, January 3, 2019

Brain regulatory T cells suppress astrogliosis and potentiate neurological recovery

So followup is needed. Contact your stroke leaders to get this done. Nothing will happen since we have NO stroke leadership.

Brain regulatory T cells suppress astrogliosis and potentiate neurological recovery

Nature (2019) | Download Citation

Abstract

In addition to maintaining immune tolerance, FOXP3⁺ regulatory T (T_reg) cells perform specialized functions in tissue homeostasis and remodelling^1,2. However, the characteristics and functions of brain T_reg cells are not well understood because there is a low number of T_reg cells in the brain under normal conditions. Here we show that there is massive accumulation of T_reg cells in the mouse brain after ischaemic stroke, and this potentiates neurological recovery during the chronic phase of ischaemic brain injury. Although brain T_reg cells are similar to T_reg cells in other tissues such as visceral adipose tissue and muscle^3,4,5, they are apparently distinct and express unique genes related to the nervous system including Htr7, which encodes the serotonin receptor 5-HT₇. The amplification of brain T_reg cells is dependent on interleukin (IL)-2, IL-33, serotonin and T cell receptor recognition, and infiltration into the brain is driven by the chemokines CCL1 and CCL20. Brain T_reg cells suppress neurotoxic astrogliosis by producing amphiregulin, a low-affinity epidermal growth factor receptor (EGFR) ligand. Stroke is a leading cause of neurological disability, and there are currently few effective recovery methods other than rehabilitation during the chronic phase. Our findings suggest that T_reg cells and their products may provide therapeutic opportunities for neuronal protection against stroke and neuroinflammatory diseases.