I posted that because that article backs many of the points that ohm made.
Really, the video that CytoDyn put on their website discussing LRM MOA in immuno-oncology also speaks to many of these points.
The tumor secretes RANTES or CCL5. CCL5 is a deceiver and recruits M2 Macrophages. NOT M1 Macrophages, M2, TAMS or Tumor Associated Macrophages.
Tregs are also recruited. Tregs are cells that turn off the immune response. Tregs are part of the immune system and they are designed to instruct Natural KIller Cells what is self and what is non-self. When the Tumor produces so much RANTES, the Tregs begin to think that the tumor is self and so the Tregs tell the NK cells and the CD8 CytoToxic T cells that the tumor and the tumor cells, circulating cells are "self" and so the NK cell moves on and leaves the tumor alone. The Tregs have been deceived and the NK cells listen to their deceived leader and leave the tumor cells alone instead of killing them.
With the upregulation of the CCR5 receptor on the surface of the tumor, TAMS and Tregs, the TAMS or the M2 Macrophages begin to produce VEGF to support angiogenesis so the tumor can survive with vascular ingrowth. M2 TAMS should be killing the tumor, but instead, they produce VEGF which brings a life line of oxygen to the tumor. RANTES is the delusion which the tumor uses to betray our own immune system.
With LRM blocking CCR5 receptors, RANTES has no effect. M2 Macrophages are converted back into M1 Macrophages which are the killing machines which should have been there destroying the tumor, not the M2 wound healing macrophage.
With LRM bound to all the CCR5, the overexpression of CCR5 subsides along with all the detrimental effects that go with overexpression. Pro-Tumor Macrophage M2 population goes down and Anti-Tumor Macrophage M1 goes up. M1 are killers, M2 are wound/tumor healing, (in NASH, they are the M2 macrophages that metabolize scar tissue in fibrosis), in cancer, they promote the tumor, so that is why LRM is so awesome, because, it is an immunomodulator, it works with both the M1, M2 and Tregs. LRM also prevents endovascular migration of the tumor cells and blocks tumor angiogenesis, VEGF is not produced by M1 Macrophage, only by M2 macrophage.
To learn the difference between M1 and M2 Macrophage Activation, see this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC...antigen%2D
ohm said more than this, but what i've said here is very important to grasp
also, take a look at this:
https://twitter.com/abushoyeb/status/15484663...74/photo/1
notice the bottom left where CCR5 is shown.
it is on a monocyte. Monocytes become Macrophages in the tissues. Monocytes are macrophages in the blood. So CCR5 is on the surfaces of these Macrophages that can either be M1, M2 or Tregs.
Really, the video that CytoDyn put on their website discussing LRM MOA in immuno-oncology also speaks to many of these points.
The tumor secretes RANTES or CCL5. CCL5 is a deceiver and recruits M2 Macrophages. NOT M1 Macrophages, M2, TAMS or Tumor Associated Macrophages.
Tregs are also recruited. Tregs are cells that turn off the immune response. Tregs are part of the immune system and they are designed to instruct Natural KIller Cells what is self and what is non-self. When the Tumor produces so much RANTES, the Tregs begin to think that the tumor is self and so the Tregs tell the NK cells and the CD8 CytoToxic T cells that the tumor and the tumor cells, circulating cells are "self" and so the NK cell moves on and leaves the tumor alone. The Tregs have been deceived and the NK cells listen to their deceived leader and leave the tumor cells alone instead of killing them.
With the upregulation of the CCR5 receptor on the surface of the tumor, TAMS and Tregs, the TAMS or the M2 Macrophages begin to produce VEGF to support angiogenesis so the tumor can survive with vascular ingrowth. M2 TAMS should be killing the tumor, but instead, they produce VEGF which brings a life line of oxygen to the tumor. RANTES is the delusion which the tumor uses to betray our own immune system.
With LRM blocking CCR5 receptors, RANTES has no effect. M2 Macrophages are converted back into M1 Macrophages which are the killing machines which should have been there destroying the tumor, not the M2 wound healing macrophage.
With LRM bound to all the CCR5, the overexpression of CCR5 subsides along with all the detrimental effects that go with overexpression. Pro-Tumor Macrophage M2 population goes down and Anti-Tumor Macrophage M1 goes up. M1 are killers, M2 are wound/tumor healing, (in NASH, they are the M2 macrophages that metabolize scar tissue in fibrosis), in cancer, they promote the tumor, so that is why LRM is so awesome, because, it is an immunomodulator, it works with both the M1, M2 and Tregs. LRM also prevents endovascular migration of the tumor cells and blocks tumor angiogenesis, VEGF is not produced by M1 Macrophage, only by M2 macrophage.
To learn the difference between M1 and M2 Macrophage Activation, see this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC...antigen%2D
ohm said more than this, but what i've said here is very important to grasp
also, take a look at this:
https://twitter.com/abushoyeb/status/15484663...74/photo/1
notice the bottom left where CCR5 is shown.
it is on a monocyte. Monocytes become Macrophages in the tissues. Monocytes are macrophages in the blood. So CCR5 is on the surfaces of these Macrophages that can either be M1, M2 or Tregs.
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