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Anti-AGO1 Antibodies Identify a Subset of Autoimmune Sensory Neuronopathy
Christian P Moritz1, Yannick Tholance2, Pierre-Baptiste Vallayer2
1From the Department of Neurology (C.P.M., P.-B.V., K.F., J.-P.C., J.-C.G.A.), University Hospital of Saint-Etienne; Synaptopathies and Autoantibodies (SynatAc) Team (C.P.M., Y.T., L.-D.D., S.M.-C., V.R., K.F., C.L.M., J.H., J.-P.C., J.-C.G.A.), Institut NeuroMyoGène, MELIS, INSERM U1314/CNRS UMR 5284, Université Claude Bernard Lyon 1; Faculty of Medicine (C.P.M., Y.T., J.-P.C., J.-C.G.A.), University Jean Monnet, Saint-Étienne, Saint-Priest-en-Jarez; Department of Biochemistry (Y.T., C.L.M.), University Hospital of Saint-Etienne; French Reference Center on Paraneoplastic Neurological Syndrome (L.-D.D., S.M.-C., V.R., J.H., J.-P.C., J.-C.G.A.), Hospices Civils de Lyon, Hôpital Neurologique, Bron; Department of Internal Medicine (M.K.), University Hospital of Saint-Etienne; CIRI-Centre International de Recherche en Infectiologie (M.K., S.P.), Team GIMAP (Saint-Etienne), Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR5308, ENS Lyon, UJM; CIC Inserm 1408 Vaccinology (M.K., S.P.), Saint-Etienne; Department of Immunology (S.P.), University Hospital of Saint-Etienne; and European Reference Center for Rare Neuromuscular Diseases (J.-P.C., J.-C.G.A.), Saint-Etienne Cedex 02, France. j.christophe.antoine@chu-st-etienne.fr.
Background And Objectives:
Autoantibodies (Abs) improve diagnosis and treatment decisions of idiopathic neurologic disorders. Recently, we identified Abs against Argonaute (AGO) proteins as potential autoimmunity biomarkers in neurologic disorders. In this study, we aim to reveal (1) the frequency of AGO1 Abs in sensory neuronopathy (SNN), (2) titers and IgG subclasses, and (3) their clinical pattern including response to treatment.
Methods:
This retrospective multicentric case/control study screened 132 patients with SNN, 301 with non-SNN neuropathies, 274 with autoimmune diseases (AIDs), and 116 healthy controls (HCs) for AGO1 Abs through ELISA. Seropositive cases were also tested for IgG subclasses, titers, and conformation specificity.
Results:
AGO1 Abs occurred in 44 patients, comprising significantly more of those with SNN (17/132 [12.9%]) than those with non-SNN neuropathies (11/301 [3.7%]; p = 0.001), those with AIDs (16/274 [5.8%]; p = 0.02), or HCs (0/116; p < 0.0001). Ab titers ranged from 1:100 to 1:100,000. IgG subclass was mainly IgG1, and 11/17 AGO1 Ab-positive SNN (65%) had a conformational epitope. AGO1 Ab-positive SNN was more severe than AGO1 Ab-negative SNN (e.g., SNN score: 12.2 vs 11.0, p = 0.004), and they more frequently and more efficiently responded to immunomodulatory treatments than AGO1 Ab-negative SNN (7/13 [54%] vs 6/37 [16%], p = 0.02). Regarding the type of treatments more precisely, this significant difference was confirmed for the use of IV immunoglobulins (IVIg) but not for steroids or second-line treatments. Multivariate logistic regression adjusted for potential confounders showed that AGO1 Ab positivity was the only predictor of response to treatment (OR 4.93, 1.10-22.24 95% CI, p = 0.03).
Discussion:
Although AGO Abs are not specific for SNN, based on our retrospective data, they may identify a subset of cases with SNN with more severe features and a possibly better response to IVIg. The significance of AGO1 Abs in clinical practice needs to be explored on a larger series.
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