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Fig. 7 | Acta Neuropathologica Communications

Fig. 7

From: Complement-independent bystander injury in AQP4-IgG seropositive neuromyelitis optica produced by antibody-dependent cellular cytotoxicity

Fig. 7

Proposed mechanisms of ADCC bystander killing in AQP4-IgG seropositive NMOSD. Diagram shows AQP4-IgG binding to AQP4 on astrocytes, with binding and activation of NK cells through Fcγ receptors. Activated NK cells can induce bystander cell damage via three mechanisms, including: (i) targeted lytic protein secretion onto immediately adjacent bystander cells following activation; (ii) sequential attack of target cells followed by release and binding/attack of a nearby bystander cell; and (iii) release of soluble granule contents following activation that then diffuse through the extracellular medium and are deposited on nearby cells

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