From one of their monkey HIV studies:

Quote:

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... CD24Fc interacts with Siglec 10/G and DAMPs to suppress DAMP-induced inflammation, confers protection in mouse models of graft vs host diseases, rheumatoid arthritis and cuprizone-induced oligodendrocyte (Li et al., 2018; Zheng et al., 2013), and is well tolerated as a drug in both human and non-human primates ...

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with references to:

https://www.nature.com/articles/cmi201747

and the patent:

https://patents.google.com/patent/US20130231464A1/en

Quote:

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The first function associated with CD24 is a costimulatory activity for antigen-specific T cell response.

Polymorphisms of human CD24 are associated with risk and progression of several autoimmune diseases, including multiple sclerosis and rheumatoid arthritis (RA). In cases of multiple sclerosis, it has been reported that soluble CD24, consisting of the extracellular portion of murine CD24 and human IgG1 Fc ameliorated the clinical symptom of experimental autoimmune diseases, the mouse model of multiple sclerosis. More recent studies have demonstrated that CD24 interact with and represses host response to danger-associated molecular patterns (DAMPs).

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So, CD24Fc blocks the DAMP innate immune response to injured cells and various inflammatory triggers indicating "danger" or "damage":

https://en.wikipedia.org/wiki/Damage-associat...ar_pattern