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Posted On: 01/25/2023 5:55:00 PM
Post# of 148899
Edit note: I didn’t mean to over emphasize the CD4/CD8 modulating concerning MS. Down regulation of Interleukins by the LL may have more consequence for MS. Interleukins are chemokines heavily activated in inflammatory responses. LL downregulates Il-6, IL-10, around a dozen others, I think. Ohm posted a list. I’m too lazy to commit much to memory. But we have many reasons to explore MS. Crossing the blood brain barrier with a reported (SK) Receptor Occupancy across the BBB of 72% I think.
From my em earlier link.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156228/
“Multiple sclerosis (MS) is a chronic inflammatory disease that is characterized by leukocyte infiltration and subsequent axonal damage, demyelinating inflammation, and formation of sclerosing plaques in brain tissue. The results of various studies in patients indicate that autoimmunity and inflammation make an important impact on the pathogenesis of MS. Chemokines are key mediators of inflammation development and cell migration, mediating various immune cell responses, including chemotaxis and immune activation, and are important in immunity and inflammation, therefore we focus on chemokines and their receptors in multiple sclerosis. In this article, we summarize the study of the role of prominent chemokines and their receptors in MS patients and MS animal modelsand discuss their potential significance in inflammatory injury and repair of MS. We have also summarized the progress in the treatment of multiple sclerosis antagonists in recent years with chemokine receptors as targets.”
And…”The hallmark of MS is leukocyte infiltration of brain tissue and subsequent axonal injury, demyelination inflammation and the formation of sclerosing plaques [54].
Abnormal inflammatory response initiated by CD4 + T cells promotes tissue damage of the CNS in EAE and MS. Among the CD4 + T cells, Th1 cells and Th17 cells are dominant, the former producing IFN-γ (interferon-γ), the latter secreting IL-17A, IL-17F, IL-21, IL-22, and GM- CSF (granulocyte–macrophage colony-stimulating factor) [60], [123]. After the secreted substances enter the central nervous system, they activate astrocytes and microglia, produce a large number of chemokines and cytokines, and recruit peripheral immune cells to sites of inflammation [123].”
From my em earlier link.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7156228/
“Multiple sclerosis (MS) is a chronic inflammatory disease that is characterized by leukocyte infiltration and subsequent axonal damage, demyelinating inflammation, and formation of sclerosing plaques in brain tissue. The results of various studies in patients indicate that autoimmunity and inflammation make an important impact on the pathogenesis of MS. Chemokines are key mediators of inflammation development and cell migration, mediating various immune cell responses, including chemotaxis and immune activation, and are important in immunity and inflammation, therefore we focus on chemokines and their receptors in multiple sclerosis. In this article, we summarize the study of the role of prominent chemokines and their receptors in MS patients and MS animal modelsand discuss their potential significance in inflammatory injury and repair of MS. We have also summarized the progress in the treatment of multiple sclerosis antagonists in recent years with chemokine receptors as targets.”
And…”The hallmark of MS is leukocyte infiltration of brain tissue and subsequent axonal injury, demyelination inflammation and the formation of sclerosing plaques [54].
Abnormal inflammatory response initiated by CD4 + T cells promotes tissue damage of the CNS in EAE and MS. Among the CD4 + T cells, Th1 cells and Th17 cells are dominant, the former producing IFN-γ (interferon-γ), the latter secreting IL-17A, IL-17F, IL-21, IL-22, and GM- CSF (granulocyte–macrophage colony-stimulating factor) [60], [123]. After the secreted substances enter the central nervous system, they activate astrocytes and microglia, produce a large number of chemokines and cytokines, and recruit peripheral immune cells to sites of inflammation [123].”
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