ReviewFrontiers in immunology2026
FcγR-ACE2 cooperative antibody-dependent enhancement in human and veterinary coronaviruses: mechanistic insights, comparative immunology, and implications for nano-engineered immunomodulatory platforms.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Antibody-dependent enhancement (ADE) is a paradoxical immunological phenomenon in which pre-existing antibodies facilitate viral entry into host cells rather than conferring protection. ADE has been extensively characterised in flaviviral systems, most notably dengue virus (DENV), and presents a significant challenge for vaccine development and antibody-based therapeutic design. In coronavirus infections, ADE may operate through both classical Fc gamma receptor (FcγR)-mediated pathways and an intrinsic signalling mechanism involving inhibitory FcγRIIb-mediated suppression of the type I interferon (IFN-I) response. Of critical translational relevance is the functionally demonstrated cooperative FcγR-ACE2 entry model for SARS-CoV-2, wherein virus-antibody immune complexes engage Fcγ receptors and require ACE2 interaction for efficient enhancement. For SARS-CoV-2 specifically, ADE magnitude appears to be determined by an antibody's capacity to block spike-ACE2 interaction rather than its neutralisation potency
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