Fig. 1.

Hypothetical models of exogenous β2-GPI-Ab interactions. Under normal conditions, the closed conformation of soluble β2-GPI is not recognized by anti-β2-GPI Ab (A). During IR-induced stress, membrane lipid alterations allow Ab recognition of bound β2-GPI (mouse protein is dark, human protein is light) and induces injury which may be exacerbated by exogenous β2-GPI (B). Excess β2-GPI may bind to altered lipids without Ab recognition (C) or exogenous β2-GPI may form soluble immunocomplexes resulting in attenuated IR-induced injury (D).