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Posted On: 06/11/2020 6:31:45 PM
Post# of 154911
Re: Rubraquercus #37441
Neuroinflammation, the accompanying amyloid plaques and damage to microglial cells are caused by an overreaction of RANTES (CCL5).
CCL5 does have a protective benefit by mediating glutamate release. CCR5 is the predominate receptor, CCL5 also binds to CCR1 and CCR3. CCR1, CCR3 and GPR75 have a lesser binding affinity for CCR5 and are expressed at a much lower level than CCR5. Thus you have a low level of CCL5 activity that allows neuroprotective glutamate mediation without the damaging inflammation.
With MCP-1 (CCL2) that is mentioned in the article which is neuroprotective (and also helps kill tumor cells) that binds to CCR2 so CCR5 blockade is not an issue.
CCL5 does have a protective benefit by mediating glutamate release. CCR5 is the predominate receptor, CCL5 also binds to CCR1 and CCR3. CCR1, CCR3 and GPR75 have a lesser binding affinity for CCR5 and are expressed at a much lower level than CCR5. Thus you have a low level of CCL5 activity that allows neuroprotective glutamate mediation without the damaging inflammation.
With MCP-1 (CCL2) that is mentioned in the article which is neuroprotective (and also helps kill tumor cells) that binds to CCR2 so CCR5 blockade is not an issue.
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