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Posted On: 06/01/2024 10:58:51 PM
Post# of 154033
Re: skipper1072 #144109
The broader takeaway is that inflammation is implicated in multiple sclerosis. But we already knew that.
FOXP1 is an anti-inflammatory that drives macrophage differentiation to an M2 anti-inflammatory phenotype. Which could accelerate EBV reproduction. That increase in FOXP1 is assuredly in response to the inflammation. What is needed is a drug that promotes killer macrophages to control EBV but also tamps down the inflammatory response. I wonder what drug can do that?
Quote:
After examining the collected samples, Dr. Lieberman and his team determined that the MS-positive samples displayed a higher level of genes associated with active EBV and inflammatory signaling, and more notably, an increase in the expression of the FOXP1 protein, which promotes EBV gene expression. This revelation provides a possible mechanism for active EBV’s contribution to inflammation and disease in MS.
https://www.msn.com/en-us/health/other/unlock...NewsSearch
FOXP1 is an anti-inflammatory that drives macrophage differentiation to an M2 anti-inflammatory phenotype. Which could accelerate EBV reproduction. That increase in FOXP1 is assuredly in response to the inflammation. What is needed is a drug that promotes killer macrophages to control EBV but also tamps down the inflammatory response. I wonder what drug can do that?
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