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Artículos de revistas sobre el tema "Anti-retinal autoantibodies"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 20 de febrero de 2023

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1

Adamus, Grazyna. "Current techniques to accurately measure anti-retinal autoantibodies". Expert Review of Ophthalmology 15, n.º 2 (3 de marzo de 2020): 111–18. http://dx.doi.org/10.1080/17469899.2020.1739522.

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2

Hooks, J. J., C. Percopo, Y. Wang y B. Detrick. "Retina and retinal pigment epithelial cell autoantibodies are produced during murine coronavirus retinopathy." Journal of Immunology 151, n.º 6 (15 de septiembre de 1993): 3381–89. http://dx.doi.org/10.4049/jimmunol.151.6.3381.

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Abstract The murine coronavirus, mouse hepatitis virus (MHV), JHM strain, induces a biphasic retinal disease in adult BALB/c mice. In the early phase of the disease, day 1 to 7, a retinal vasculitis is noted and is associated with the presence of virus particles. In the late phase of the disease, day 10 to 140, a retinal degeneration is observed and is associated with the absence of both virus particles and inflammatory cells. We show that the retinal degenerative process is also associated with the presence of antiretinal autoantibodies. In total, 22 of 23 sera collected from 10 to 70 days after JHM virus inoculation contained antiretinal autoantibodies. These autoantibodies are not found in sera from normal or mock-injected mice. Antibodies to retinal tissue were identified as two distinct patterns of immunoperoxidase staining on frozen sections of normal rat eyes, retinal autoantibodies and retinal pigment epithelium (RPE) autoantibodies. The antiretinal autoantibodies first appeared as IgM class antibodies that shifted to IgG class autoantibodies. The anti-RPE cell autoantibodies were predominantly of the IgG class. Sera that were positive for these autoantibodies did not stain with liver or kidney sections but 2 of 3 did react with rat brain sections. A second mouse strain, CD-1, was also evaluated because these animals respond to JHM virus inoculation by developing only the early phase of this disease, i.e. vasculitis. On day 10 postinoculation, the retina architecture has a normal appearance. In these mice, which are free of a retinal degeneration, antiretinal autoantibodies are not produced. However, just as is noted in the BALB/c mice, antivirus neutralizing antibodies are produced in the infected CD-1 mice. These findings suggest a role for autoimmunity in the pathogenesis of murine coronavirus induced retinal degeneration. This study establishes an animal model for the study of humoral autoimmune responses in human retinal degenerations.

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3

Garweg, Justus G., Yvonne de Kozak, Brigitte Goldenberg y Matthias Boehnke. "Anti-retinal autoantibodies in experimental ocular and systemic toxoplasmosis". Graefe's Archive for Clinical and Experimental Ophthalmology 248, n.º 4 (3 de diciembre de 2009): 573–84. http://dx.doi.org/10.1007/s00417-009-1242-z.

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4

Cheung, C. M. G. y S. P. Chee. "Anti-retinal autoantibodies-positive autoimmune retinopathy in cytomegalovirus-positive anterior uveitis". British Journal of Ophthalmology 94, n.º 3 (1 de marzo de 2010): 380–81. http://dx.doi.org/10.1136/bjo.2009.170464.

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5

Adamus, Grazyna, Rachel Champaigne y Sufang Yang. "Occurrence of major anti-retinal autoantibodies associated with paraneoplastic autoimmune retinopathy". Clinical Immunology 210 (enero de 2020): 108317. http://dx.doi.org/10.1016/j.clim.2019.108317.

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6

Shinohara, Yoichiro, Ryo Mukai, Shinji Ueno y Hideo Akiyama. "Clinical Findings of Melanoma-Associated Retinopathy with anti-TRPM1 Antibody". Case Reports in Ophthalmological Medicine 2021 (8 de septiembre de 2021): 1–5. http://dx.doi.org/10.1155/2021/6607441.

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Introduction. We report the clinical features and clinical course of melanoma-associated retinopathy (MAR), in which autoantibodies against the transient receptor potential cation channel subfamily M member 1 (TRPM1) were detected. Case Presentation. A 74-year-old man was referred to our hospital for treatment of bilateral vision loss. The best-corrected visual acuity was 20/100 in the right eye and 20/200 in the left eye. His electroretinogram (ERG) showed a reduced b-wave and a normal dark-adapted a-wave in both eyes. Optical coherence tomography (OCT) revealed loss of the interdigitation zone in both eyes. We strongly suspected MAR based on the markedly reduced b-wave in the ERG and a history of intranasal melanoma. The diagnosis was confirmed after autoantibodies against TRPM1 were detected in his blood serum. Fifteen months later, his ERG remained unchanged, and OCT showed bilateral cystic changes in the internal nuclear layer. The visual acuity in both eyes also remained unchanged. Conclusions. Anti-TRPM1 autoantibodies were detected in a patient diagnosed with MAR who had negative flash ERG and retinal microstructural abnormalities, and the impairment did not recover during the follow-up period. Identification of anti-TRPM1 antibodies was helpful in confirming the diagnosis of MAR.

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7

Hurez, Vincent, Michel D. Kazatchkine, Tchavdar Vassilev, Sheela Ramanathan, Anastas Pashov, Bertrand Basuyaux, Yvonne de Kozak, Blanche Bellon y Srini V. Kaveri. "Pooled Normal Human Polyspecific IgM Contains Neutralizing Anti-Idiotypes to IgG Autoantibodies of Autoimmune Patients and Protects From Experimental Autoimmune Disease". Blood 90, n.º 10 (15 de noviembre de 1997): 4004–13. http://dx.doi.org/10.1182/blood.v90.10.4004.

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Abstract Normal human serum contains IgM antibodies that regulate the natural autoantibody activity of IgG in autologous serum. In the present study, we show that pooled normal human IgM (IVIgM) purified from plasma of more than 2,500 healthy donors and processed in a similar fashion to that of therapeutic preparations of pooled normal human IgG (IVIg) suppresses activity of IgG autoantibodies purified from the serum of patients with autoimmune diseases in vitro. The inhibitory effect of IVIgM was greater or equivalent to that of IVIg on a molar basis. We show that IVIgM contains anti-idiotypic antibodies directed against idiotypic determinants of autoantibodies, in particular by showing that Sepharose-bound IVIgM selectively retained F(ab′)2 fragments of IgG autoantibodies. The infusion of (Lewis × Brown-Norway) F1 rats with IVIgM protected the animals against experimental autoimmune uveitis induced by immunization with the soluble retinal S antigen, as evidenced by clinical scoring and histopathological analysis. The present findings provide a rationale for considering pooled IgM for immunomodulation of autoimmune disease.

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8

Adamus, G., D. Amundson, G. M. Seigel y M. Machnicki. "Anti-Enolase-α Autoantibodies in Cancer-Associated Retinopathy: Epitope Mapping and Cytotoxicity on Retinal Cells". Journal of Autoimmunity 11, n.º 6 (diciembre de 1998): 671–77. http://dx.doi.org/10.1006/jaut.1998.0239.

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9

Khaddour, Karam, Sangeeta Khanna, Michael Ansstas, Ishaan Jakhar, Sonika Dahiya, Laurin Council y George Ansstas. "Normalization of electroretinogram and symptom resolution of melanoma-associated retinopathy with negative autoantibodies after treatment with programmed death-1 (PD-1) inhibitors for metastatic melanoma". Cancer Immunology, Immunotherapy 70, n.º 9 (5 de febrero de 2021): 2497–502. http://dx.doi.org/10.1007/s00262-021-02875-x.

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AbstractMelanoma-associated retinopathy (MAR) is a paraneoplastic syndrome that involves the production of autoantibodies which can cross-react with retinal epitopes leading to visual symptoms. Autoantibodies can target intracellular proteins, and only a few are directed against membrane proteins. This discrepancy in autoantibody–protein target can translate into different immune responses (T-cell mediated vs B-cell mediated). Historically, treatment of MAR has focused on surgical reduction or immunosuppressive medication, mainly glucocorticoids. However, tumor resection is not relevant in metastatic melanoma in which MAR is mostly encountered. Moreover, the use of glucocorticoids can reduce the efficacy of immunotherapy. We report the first case to our knowledge with subjective resolution of visual symptoms and objective evidence of normalization of electroretinogram of MAR with undetectable autoantibodies after administration of programmed death-1 (PD-1) inhibitor (pembrolizumab) without the use of surgical reduction or systemic immunosuppression. This case highlights the potential improvement and resolution of negative autoantibody MAR with the use of PD-1 inhibitors and emphasizes the importance of multidisciplinary approach and team discussion to avoid interventions that can decrease immunotherapy-mediated anti-tumor effect.

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10

Gyoten, Daichi, Shinji Ueno, Satoshi Okado, Taro Chaya, Shunsuke Yasuda, Takeshi Morimoto, Mineo Kondo et al. "Broad locations of antigenic regions for anti-TRPM1 autoantibodies in paraneoplastic retinopathy with retinal ON bipolar cell dysfunction". Experimental Eye Research 212 (noviembre de 2021): 108770. http://dx.doi.org/10.1016/j.exer.2021.108770.

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11

Piantoni, S., F. Regola, S. Masneri, C. Nalli, C. Bazzani, C. Rossini, G. Chiarini et al. "POS0593 THE REDUCTION OF RETINAL MICROVASCULAR ALTERATIONS AND THE DECREASE OF A POTENTIALLY RELATED T-CELL SUBSET IN PATIENTS WITH ACTIVE RHEUMATOID ARTHRITIS TREATED WITH ABATACEPT". Annals of the Rheumatic Diseases 80, Suppl 1 (19 de mayo de 2021): 530.1–530. http://dx.doi.org/10.1136/annrheumdis-2021-eular.483.

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Background:T-cells play a pivotal role in the pathogenesis of rheumatoid arthritis (RA) and in its cardiovascular (CV) comorbidities, acting at microvascular level [1]. Since small artery remodeling is the earliest form of target organ damage in hypertension, the evaluation of microvascular alterations might provide clinically useful information. The evaluation of retinal arterioles is a non-invasive technique to identify a precocious microvascular damage, which is related to an increase of the wall-to-lumen ratio (WLR) [2]. CD3+CD31+CXCR4+ T-cells may be involved in damaged endothelium repair and are increased in patients with morphological microvascular alterations [3]. In addition to its effect on disease activity, abatacept (ABA), a co-stimulator blocker which is approved for the treatment of RA, may have specific CV protective action, modulating the numbers of certain subtypes of lymphocytes [4].Objectives:To non-invasively investigate morphological characteristics of retinal arterioles and to evaluate CD3+CD31+CXCR4+T-cells in a cohort of RA patients treated with ABA.Methods:Eleven RA patients [median (25th-75thpercentile) age=58 (50-65) years, baseline C-reactive protein (CRP)-DAS28=4.4 (3.8-4.6), body mass index (BMI)=23.4 (21.6-25.6) kg/m2, rheumatoid factor (RF) positive:45%, anti-citrullinated peptide autoantibodies (ACPA) positive:73%] without known CV risk factors (arterial hypertension, diabetes, hypercholesterolemia, previous CV events, smoking) were evaluated by adaptive optics, a validated technique quantifying microvascular damage [5], before and every 6 months of therapy with ABA (T0, T6 and T12). Phenotypic analysis of peripheral blood T lymphocytes was made by flow-cytometry in 5 patients of the cohort at T0 and T6.Results:A progressive significant reduction of the WLR of retinal arterioles was observed [T0=0.28 (0.25-0.30), T6=0.27 (0.24-0.31), T12=0.23 (0.23-0.26); p T0 vs T6=0.4; p T6 vs T12=0.01; p T0 vs T12=0.01] (Figure 1), without significant variations in the other parameters [internal diameter: T0=94.4 (84.1-104.0), T6=94.8 (84.6-107.7), T12=99.2 (89.1-109.1) µm; external diameter: T0=125.8 (111.1-131.0), T6=122.4 (109.1-134.5), T12=125.6 (113.9-134.4) µm; wall thickness: T0=13.2 (12.2-14.4), T6=13.4 (11.7-14.4), T12=12.5 (11.6-13.0) µm; wall cross-sectional area: T0=4581.0 (3788.7-5263.7), T6=4563.3 (3788.5-5295.2), T12=4099.7 (3899.0-5145.7) µm2)]. In 5 patients evaluated also for T-cell immunophenotyping a negative correlation was observed between CD3+CD31+CXCR4+ T-cell number and the retinal wall thickness at baseline (R=0.871;p=0.05). After ABA therapy a trend for reduction of CD3+CD31+CXCR4+T-cells [19.0 (13.8-38.3) vs 12.4 (5.2-18.0) % of CD3+], was observed as well as of significant reduction of retinal wall cross-sectional area [5123.3 (4385.0-5470.3) vs 4852.3 (4118.3-5228.0) µm2;p=0.04].Conclusion:In a cohort of RA patients without known CV risk factors, a reduction in retinal microvascular alterations arterioles was demonstrated after treatment for 12 months with ABA. CD3+CD31+CXCR4+T-cell number was inversely related to the possible presence of subclinical CV involvement. These results may suggest the possibility of microvascular abnormalities regression induced by the immune system modulation.References:[1]Dessein PH, J Rheumatol 2005.[2]Rizzoni D, Am J Hypertens. 2018.[3]Hur J, Circulation 2007.[4]Kallikourdis M, Nat Commun 2017.[5]De Ciuceis C, J Hypertens 2018.Acknowledgements:Bristol-Myers-Squibb Italy provided an unrestricted research grant for the study conduct.Figure 1.Disclosure of Interests:None declared

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12

Sim, Shaun Sebastian, Chee Wai Wong, Quan V. Hoang, Shu Yen Lee, Tien Yin Wong y Chui Ming Gemmy Cheung. "Anti-retinal autoantibodies in myopic macular degeneration: a pilot study". Eye, 28 de octubre de 2020. http://dx.doi.org/10.1038/s41433-020-01241-y.

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13

Adamus, Grazyna. "Are Anti-Retinal Autoantibodies a Cause or a Consequence of Retinal Degeneration in Autoimmune Retinopathies?" Frontiers in Immunology 9 (16 de abril de 2018). http://dx.doi.org/10.3389/fimmu.2018.00765.

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14

Adamus, Grazyna. "Significance of Anti-retinal Autoantibodies in Cancer-associated Retinopathy with Gynecological Cancers". Journal of Clinical & Experimental Ophthalmology 04, n.º 06 (2013). http://dx.doi.org/10.4172/2155-9570.1000307.

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15

Adamus, Grazyna, Emily Y. Chew, Frederick L. Ferris y Michael L. Klein. "Prevalence of anti-retinal autoantibodies in different stages of Age-related macular degeneration". BMC Ophthalmology 14, n.º 1 (diciembre de 2014). http://dx.doi.org/10.1186/1471-2415-14-154.

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16

Pawestri, Aulia Rahmi, Niracha Arjkongharn, Ragkit Suvannaboon, Aekkachai Tuekprakhon, Vichien Srimuninnimit, Suthipol Udompunthurak, La-ongsri Atchaneeyasakul, Ajchara Koolvisoot y Adisak Trinavarat. "Autoantibody profiles and clinical association in Thai patients with autoimmune retinopathy". Scientific Reports 11, n.º 1 (22 de julio de 2021). http://dx.doi.org/10.1038/s41598-021-94377-0.

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AbstractAutoimmune retinopathy (AIR) is a rare immune-mediated inflammation of the retina. The autoantibodies against retinal proteins and glycolytic enzymes were reported to be involved in the pathogenesis. This retrospective cohort study assessed the antiretinal autoantibody profiles and their association with clinical outcomes of AIR patients in Thailand. We included 44 patients, 75% were females, with the overall median age of onset of 48 (17–74, IQR 40–55.5) years. Common clinical presentations were nyctalopia (65.9%), blurred vision (52.3%), constricted visual field (43.2%), and nonrecordable electroretinography (65.9%). Underlying malignancy and autoimmune diseases were found in 2 and 12 female patients, respectively. We found 41 autoantibodies, with anti-α-enolase (65.9%) showing the highest prevalence, followed by anti-CAII (43.2%), anti-aldolase (40.9%), and anti-GAPDH (36.4%). Anti-aldolase was associated with male gender (P = 0.012, OR 7.11, 95% CI 1.54–32.91). Anti-CAII showed significant association with age of onset (P = 0.025, 95% CI − 17.28 to − 1.24), while anti-α-enolase (P = 0.002, OR 4.37, 95% CI 1.83–10.37) and anti-GAPDH (P = 0.001, OR 1.87, 95% CI 1.32–2.64) were significantly associated with nonrecordable electroretinography. Association between the antibody profiles and clinical outcomes may be used to direct and adjust the treatment plans and provide insights in the pathogenesis of AIR.

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17

van Romunde, Saskia H. M., Daphne P. C. Vergouwen, Daniela Iacovello, Dave L. Roelen, Robert M. Verdijk, Josianne C. E. M. ten Berge, Grazia Pertile, Marco W. J. Schreurs y Jan C. van Meurs. "Destructive inflammatory reaction after an autologous retinal pigment epithelium and choroid transplantation: no detection of an auto-immune response". Journal of Ophthalmic Inflammation and Infection 12, n.º 1 (26 de agosto de 2022). http://dx.doi.org/10.1186/s12348-022-00305-2.

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Abstract Purpose Five patients who underwent uncomplicated retinal pigment epithelium (RPE)-choroid transplantation for neovascular age-related macular degeneration developed a destructive inflammatory reaction causing subretinal fluid accumulation and extensive RPE atrophy in the graft. We hypothesized that this inflammation could be caused by an auto-immune response against the graft, resulting in circulating auto-antibodies. The aim of our study was to examine a potential autoimmune origin, which would allow a more targeted therapy approach. Methods Five above-mentioned patients and four control groups of five patients each were included: 1) after uncomplicated RPE-choroid transplantation, 2) after full macular translocation, 3) treated with anti-vascular endothelial growth factor, and 4) healthy controls. Histopathology of rejected graft tissue was performed using standard procedures. Presence of RPE-choroid autoantibodies in serum was examined by indirect immunofluorescence and Western blot, and human leukocyte antigen (HLA) typing was performed. Results Histopathological examination of an explanted graft showed infiltration of T-lymphocytes and macrophages in the choroid and RPE, and an increased number of B-cell lymphocytes were found in the choroid. Indirect immunofluorescence showed weak RPE-choroid autoantibody immunoreactivity in three patients of different groups. Western blot did not show specific RPE-choroid autoantibody immunoreactivity and no difference of HLA genotypes between the groups was found. Conclusions Although local mononuclear inflammatory cell infiltration and a high number of B-lymphocytes were observed in an explanted graft, we did not detect serological evidence of an autoimmune origin of the postoperative inflammation using direct immunofluorescence and Western Blot. Alternatively, the graft failure may have been caused by local innate inflammation, triggered by breakdown of tolerance. Based on our current findings of this small study group, we have no rationale to pursue therapies targeted towards autoreactive graft failure. More research is needed to confirm our findings.

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