Lack of KIR4.1 autoantibodies in Japanese patients with MS and NMO. Higuchi O, Nakane S, Sakai W, Maeda Y, Niino M, Takahashi T, Fukazawa T, Kikuchi S, Fujihara K, Matsuo H. Neurol Neuroimmunol Neuroinflamm. 2016 Jul 22;3(5):e263. doi: 10.1212/NXI.0000000000000263. eCollection 2016 Oct.
OBJECTIVES:To examine anti-KIR4.1 antibodies by 2 different assays in Japanese patients with multiple sclerosis (MS) or neuromyelitis optica (NMO).
METHODS:One hundred sixty serum samples from 57 patients with MS, 40 patients with NMO/NMO spectrum disorder (NMOSD), and 50 healthy controls (all were Japanese) were tested with ELISA using a synthetic peptide of the first extracellular portion of human KIR4.1. In addition, we attempted to detect anti-KIR4.1 immunoglobulin G in the serum by the luciferase immunoprecipitation systems (LIPS) with the full length of human KIR4.1 produced in a human cell line, which is highly sensitive to single or multiple epitopes.
RESULTS:We failed to detect antibodies to the peptide fragment KIR4.1(83-120) in any case of MS and NMO/NMOSD using ELISA. Antibodies to the recombinant full length of KIR4.1 protein were detected in only 2 patients with MS and none in the patients with NMO/NMOSD by the LIPS assay.
CONCLUSIONS:We developed 2 different methods (ELISA and LIPS) to measure autoantibodies to KIR4.1 in serum. We detected anti-KIR4.1 immunoglobulin G at a very low frequency in Japanese patients with MS or NMO/NMOSD. Serologic testing for human KIR4.1-specific antibodies is unlikely to improve the diagnosis of MS or NMO/NMOSD in Japanese patients.
It was claimed that over 50% of people with MS had antibodies to this potassium channel, implying that this is a cause of autoimmunity. This paper says no they don’t as have a load of other papers questioning the validity of the original observation. It shows the importance of replication, but such studies take about 5 or so other studies to correct the original idea