Anti-Enolase-α Autoantibodies in Cancer-Associated Retinopathy: Epitope Mapping and Cytotoxicity on Retinal Cells

Adamus, Grażyna; Amundson, Drake; Seigel, Gail M.; Machnicki, Michał

doi:10.1006/jaut.1998.0239

Cited by 112 publications

(87 citation statements)

References 18 publications

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“…5 It is not clear why autoantibodies against a-enolase and other proteins involved in cell functions are found in human plasma, but one possible mechanism of a-enolase autoantibody induction is as follows: in the lung adenocarcinoma patients, a-enolase was found to be massively expressed in cancer cells, and thus might have required the autoantibody to neutralize its side-effect. There have been many reports on the presence of a-enolase autoantibody in patients with various diseases, such as Hashimoto's encephalopathy, 16 cancer-associated retinopathy 17 and discoid lupus erythematosus. 18 Therefore, abnormally growing cancer cells may be a potential source of a-enolase as an autoantigen in various cancers.…”

Section: Discussionmentioning

confidence: 99%

Identification of L-plastin autoantibody in plasma of patients with non-Hodgkin's lymphoma using a proteomics-based analysis

et al. 2008

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Background: The diagnosis of malignant lymphoma (ML) such as non-Hodgkin's lymphoma (NHL) and Hodgkin's lymphoma (HL) was mainly performed by morphological examination and gene analysis. There are only a few serum/plasma biomarkers such as lactate dehydrogenase and soluble interleukin-2 receptor a to diagnose ML. The classifications are various, and therefore the cell surface markers using flow cytometry or lymph node biopsy have been examined. It is difficult, however, to distinguish the two diseases, NHL and HL, from each other. Methods: In order to identify the haematological malignancy-associated autoimmunoreactivity (autoantibodies) in patients' plasma, a novel proteomics-based approach using electrophoresis/mass spectrometry was applied. Solubilized proteins from a Burkitt's lymphoma cell line (Raji) were separated by sodium dodecyl sulphate-polyacrylamide gel electrophoresis and Western blotting analysis, in which the plasma of individual patients with haematological malignancies was tested for primary antibodies, followed by visualization with anti-IgG antibody conjugated with horseradish peroxidase. Results: Two proteins, L-plastin and a-enolase, capable of reacting with the antibodies in plasma of patients with NHL, were detected using matrix-assisted laser desorption ionization/time-of-flight mass spectrometry and tandem mass spectrometry. The rates of the detections of an anti L-plastin autoantibody were significantly higher: 0.84 (21/25) in patients with NHL; 0.00 (0/4) in HL; 0.38 (5/13) in autoimmune diseases; 0.20 (2/10) in leukaemia; and 0.13 (1/8) in healthy controls. In contrast, those of anti a-enolase antibody were not specific to NHL. Conclusions: We first identified autoantibody against L-plastin in plasma of patients with NHL, suggesting that the autoantibody can be a new diagnostic biomarker for NHL.

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Section: Discussionmentioning

confidence: 99%

Identification of L-plastin autoantibody in plasma of patients with non-Hodgkin's lymphoma using a proteomics-based analysis

et al. 2008

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“…Enolase is another metabolic enzyme which is potentially interesting in the context of MS. Antibodies against non-neuronal enolase (NNE) have been described in various autoimmune diseases, where they are believed to have a pathological role (6,7). Autoantibodies against NNE have also been implicated as a cause of autoimmune retinopathy (8)(9)(10). We, and others have reported the presence of anti-NNE antibodies in association with retinopathy in MS patients (11,12).…”

Section: Introductionmentioning

confidence: 98%

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

et al. 2007

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Introduction-Although myelin autoimmunity is known to be a major factor in the pathogenesis of multiple sclerosis (MS), the role of nonmyelin antigens is less clear. Given the complexity of this disease, it is possible that autoimmunity against nonmyelin antigens also has a pathogenic role. Autoantibodies against enolase and arrestin have previously been reported in MS patients. The Tcell response to these antigens, however, has not been established.

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“…[34][35][36][37][38][39] Both in vitro and in vivo studies have also demonstrated the retinal toxicity of autoantibodies against α-enolase through similar caspase-dependent apoptotic mechanisms. [40][41][42] Autoantibodies targeting various other retinal proteins have also been implicated as putative causative agents based on the identification of these antibodies in the serum of patients with presumed AIR. These include antibodies against carbonic anhydrase II (which is abundant in ocular tissues) 17,43,44 and the retina-specific tubby-like protein 1 (TULP1).…”

Section: Antiretinal Antibodies: Pathogenic Uncertaintiesmentioning

confidence: 99%

“…Cell culture studies have suggested that anti-α-enolase antibodies from patients with CAR recognize specific epitopes that are not recognized by anti-α-enolase antibodies from healthy patients. 42 However, this still does not adequately explain why the toxicity of anti-α-enolase antibodies should be limited to the retina, as α-enolase is ubiquitous in humans. 51 It is possible that these autoantibodies are simply an epiphenomenon, and are indeed not pathogenic.…”

Section: Antiretinal Antibodies: Pathogenic Uncertaintiesmentioning

confidence: 99%