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Shown are membrane-bound hemichromes (panel A), complement C3c fragment (panel B) and autologous IgG (panel C) in ring-infected and non-infected GR-deficient RBCs from the index patient, brother (individual 2) and sister (individual 3) of index patient, and from normal GR-sufficient controls
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Surprisingly, this is not due to heme-induced activation of HRI, but rather triggered by DELE1, although there are some key differences with the established model
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