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. 2020 Dec 31;22(1):389. doi: 10.3390/ijms22010389

Figure 1.

Figure 1

Antibodies and their pathogenic effects in limbic encephalitis. The pathologic effects of antibodies include blocking of receptors or ion channels, disruption of interaction with neighboring molecules, and crosslinking and internalization of receptors from cell surface. (1) CASPR2 and contactin2 antibodies inhibit the interaction between these proteins and reduce the clustering and surface expression of VGKC; (2) LGI1 antibody disrupts interaction between protein components such as LGI1 to ADAM22/23, downregulates VGKC and reduces AMPAR clustering and synaptic transmission; (3) AMPAR antibody causes cross-linking and receptor internalization; (4) NMDAR* antibody causes cross-linking and receptor internalization; (5) mGluR5 antibody causes decreased synaptic mGluR5 cluster density; (6) GAD antibodies target mostly the GAD65 subunits but also the GAD67 subunits, disrupting GABAergic signaling; (7) GABA-BR antibody prevents ligand binding to the receptor and alters receptor function; (8) GlyR antibody probably acts as antagonist to disrupt receptor function. Ab: antibody; ADAM: a disintegrin and metalloproteinase; AMPAR: α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor; CASPR2: contactin associated protein-like 2; GABA-AR: γ-aminobutyric acid-A receptor; GABA-BR: γ-aminobutyric acid-B receptor, GAD: glutamic acid decarboxylase; GlyR: glycine receptor; LGI1: leucine-rich, glioma inactivated 1; mGluR5: metabotropic glutamate receptor 5; NMDAR: N-methyl-D-asparate receptor; PSD-95: postsynaptic density protein 95; VGKC: voltage-gated potassium channels.