Figure 2. Detection of KIR4.1 autoantibodies using LIPS

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Figure 1 Percent positivity by clinical feature Overall, 6
FL cells are dependent on BCL6 in a NOTCH2-dependent manner.
Figure 2 Expression of GABAA receptor and LGI1 by patient's thymomaTissue sections of the patient's thymoma incubated with biotinylated immunoglobulin.
Figure 1 Reactivity of the patients' antibodies with rat brain and HEK cell-based assays Rat hippocampal dentate gyrus neuropils were stained with patient.
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Figure 1 Neuromyelitis optica spectrum disorder (NMOSD) subgroups and patients with relapsing-remitting multiple sclerosis (RRMS) show different antibody.
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Figure 2. Detection of KIR4.1 autoantibodies using LIPS Detection of KIR4.1 autoantibodies using LIPS (A) LIPS assay for KIR4.1 by rabbit antiserum for the KIR4.192–105 peptide. Anti-KIR4.1 antibodies bound KIR4.1-GL in a dose-dependent manner. The x-axis indicates the amount of antiserum for the KIR4.192–105 peptide. The y-axis indicates KIR4.1-GL activity. The lines with open and closed circles are the results using preimmune serum and antiserum for the KIR4.192–105 peptide, respectively. (B) LIPS assay for KIR4.1. Two patients with multiple sclerosis were positive for the anti-KIR4.1 antibody based on the LIPS assay (3.3%); none of the patients with NMO or NMOSD, or HCs, were autoantibody-positive. There were no statistical differences among the 3 groups (p = 0.469). The y-axis indicates the luciferase activity of KIR4.1-GL (in RLU). Red and black lines indicate the cutoff value and the mean values, respectively. GL = Gaussia luciferase; HC = healthy controls. KIR4.1 = inward rectifying potassium channel 4.1; LIPS = luciferase immunoprecipitation systems; NMO = neuromyelitis optica; NMOSD = NMO spectrum disorder; RLU = relative luminescence units. Osamu Higuchi et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e263 © 2016 American Academy of Neurology