Oncoimmune's CD24Fc, as best I am able to determin
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Posted On: 12/23/2020 11:53:09 AM
Oncoimmune's CD24Fc, as best I am able to determine, blocks the activation of the innate immune system via Pathogen Associatated Molecur Pathways (PAMPS) and Damage Associated Molecular Pathways (DAMPS), but will fall short when immune dysregulation has developed with excessive trafficking of monocytes to areas of inflammation and hyper-inflammation.
Monocyte activation and trafficking are key mechanisms that magnify the innate immune response to damaging levels. Blockade of macrophage activation (CCL3 & CCL4) and macrophage chemoattractant protein (CCL2 and CCL5/RANTES) are required to restore appropriate immune functioning.
Attempting to correct the immune dysregulation of severe Covid is akin to stopping a raging forest fire by confiscating matches and lighters.
http://www.oncoimmune.com/index.php?option=co...Itemid=426
Pattern recognition receptors, such as Toll or Toll-like receptors (TLRs), recognize pathogens (Pathogen-Associated Molecular Patterns, or PAMPs) or components of injured cells (Danger-Associated Molecular Patterns, or DAMPs), and trigger activation of the innate immune system. On the other hand, Siglecs are a distinct class of pattern recognition receptors that down-regulate cellular responses. As reported by our Founders in Science (2009) and Nature Biotech (2011), CD24 interacts with DAMPs as well as a pattern recognition receptor, which is called Siglec G in mice and Siglec 10 in human, to selectively regulate host responses to DAMPs.
Specifically, the CD24-Siglec-G (or its human homologue, Siglec 10) interaction negatively regulates the activity of NFkB via intracellular ITIM domains that are associated with SHP-1. Accordingly, binding of CD24 to Siglec G/10 suppresses TNF-α, IL-1β and IL-6, which are all major targets of autoimmune diseases and cancer. Furthermore, CD24 binds to several DAMPs and represses host response to these DAMPs.
Therefore, CD24Fc has a dual mechanism of action:
CD24Fc binds DAMPs, trapping the inflammatory stimuli to prevent their interaction with TLR receptors
CD24Fc binds Siglec G/10 and regulates host response to tissue injuries Siglec G/10-associated SHP1 inhibitory signaling
Monocyte activation and trafficking are key mechanisms that magnify the innate immune response to damaging levels. Blockade of macrophage activation (CCL3 & CCL4) and macrophage chemoattractant protein (CCL2 and CCL5/RANTES) are required to restore appropriate immune functioning.
Attempting to correct the immune dysregulation of severe Covid is akin to stopping a raging forest fire by confiscating matches and lighters.
http://www.oncoimmune.com/index.php?option=co...Itemid=426
Pattern recognition receptors, such as Toll or Toll-like receptors (TLRs), recognize pathogens (Pathogen-Associated Molecular Patterns, or PAMPs) or components of injured cells (Danger-Associated Molecular Patterns, or DAMPs), and trigger activation of the innate immune system. On the other hand, Siglecs are a distinct class of pattern recognition receptors that down-regulate cellular responses. As reported by our Founders in Science (2009) and Nature Biotech (2011), CD24 interacts with DAMPs as well as a pattern recognition receptor, which is called Siglec G in mice and Siglec 10 in human, to selectively regulate host responses to DAMPs.
Specifically, the CD24-Siglec-G (or its human homologue, Siglec 10) interaction negatively regulates the activity of NFkB via intracellular ITIM domains that are associated with SHP-1. Accordingly, binding of CD24 to Siglec G/10 suppresses TNF-α, IL-1β and IL-6, which are all major targets of autoimmune diseases and cancer. Furthermore, CD24 binds to several DAMPs and represses host response to these DAMPs.
Therefore, CD24Fc has a dual mechanism of action:
CD24Fc binds DAMPs, trapping the inflammatory stimuli to prevent their interaction with TLR receptors
CD24Fc binds Siglec G/10 and regulates host response to tissue injuries Siglec G/10-associated SHP1 inhibitory signaling
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