High incidence of antibodies to lens proteins in sera from patients with uveitis

Doycheva, Deshka; Preuß, B.; Klein, Reinhild; Zierhut, Manfred

doi:10.1007/s00417-006-0407-2

Cited by 5 publications

(4 citation statements)

References 39 publications

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“…For instance antibodies against α -enolase have been associated not only with AMD [ 42 ] but also with cancer associated retinopathy (CAR) and nonparaneoplastic autoimmune retinopathy (npAIR) [ 35 , 50 , 51 ]. Similarly, antibodies specific for α B-crystallin, which is the basic structural component of multiple heat chock proteins (HSP), are found not only in sera of AMD patients [ 42 ] but also in sera of patients with uveitis [ 52 ]. Moreover, α -crystallin is also recognized by autoantibodies during multiple sclerosis [ 53 ] and cardiovascular diseases [ 54 ].…”

Section: Role Of Antiretinal and Anti-rpe Autoantibodies Found In mentioning

confidence: 99%

Potential Sources and Roles of Adaptive Immunity in Age-Related Macular Degeneration: Shall We Rename AMD into Autoimmune Macular Disease?

Camelo¹

2014

Autoimmune Diseases

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Age-related macular degeneration (AMD) is the leading cause of vision loss in the elderly throughout the industrialized world. Its most prominent pathologic features are lesions involving the retinal pigment epithelium (RPE) the Bruch's membrane, the degeneration of photoreceptors, and, in the most aggressive cases, choroidal neovascularization. Genetic associations between the risk of developing AMD and polymorphism within components of the complement system, as well as chemokine receptors expressed on microglial cells and macrophages, have linked retinal degeneration and choroidal neovascularization to innate immunity (inflammation). In addition to inflammation, players of the adaptive immunity including cytokines, chemokines, antibodies, and T cells have been detected in animal models of AMD and in patients suffering from this pathology. These observations suggest that adaptive immunity might play a role in different processes associated with AMD such as RPE atrophy, neovascularization, and retinal degeneration. To this date however, the exact roles (if any) of autoantibodies and T cells in AMD remain unknown. In this review we discuss the potential effects of adaptive immune responses in AMD pathogenesis.

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Section: Role Of Antiretinal and Anti-rpe Autoantibodies Found In mentioning

confidence: 99%

Potential Sources and Roles of Adaptive Immunity in Age-Related Macular Degeneration: Shall We Rename AMD into Autoimmune Macular Disease?

Camelo¹

2014

Autoimmune Diseases

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“…1 x 10 8 PBMC were washed (4°C, 500 x g, 10 min) and then resuspended in 10 ml MACS buffer (phosphate-buffered saline (pH 7.2), supplemented with 2 mM EDTA (AppliChem, Darmstadt, Germany) and 0.5% bovine serum albumin (Serva, Heidelberg, Germany)). After another washing step, cells were incubated at 4°C with 1 ml mouse anti horse CD4 antibody (clone MCA 1078, Biorad, Feldkirchen, Germany, 1:2000) per 1x10 7 cells. After 20 minutes, 5 ml MACS buffer were added for washing (4°C, 500 x g, 10 min).…”

Section: Magnetic Activated Cell Sorting (Macs) Of Cd4 + T Cells Using Ls Columnsmentioning

confidence: 99%

“…Like in other autoimmune diseases, the pathogenesis of ERU is still not fully elucidated (1,6). ERU represents the only spontaneous animal model for human autoimmune uveitis (HAU), a sight-threatening disease with a similar pathogenesis as ERU (1,(7)(8)(9). Thus, new findings concerning the underlying pathogenesis of ERU are of great value for both, veterinary and human medicine.…”

Section: Introductionmentioning

confidence: 99%

Altered Metabolic Phenotype of Immune Cells in a Spontaneous Autoimmune Uveitis Model

et al. 2021

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As one of the leading causes of blindness worldwide, uveitis is an important disease. The exact pathogenesis of autoimmune uveitis is not entirely elucidated to date. Equine recurrent uveitis (ERU) represents the only spontaneous animal model for autoimmune uveitis in humans. As the metabolism of immune cells is an emerging field in research and gains more and more significance to take part in the pathogenesis of various diseases, we conducted experiments to investigate the metabolism of immune cells of ERU cases and healthy controls. To our knowledge, the link between a deviant immunometabolism and the pathogenesis of autoimmune uveitis was not investigated so far. We showed that PBMC of ERU cases had a more active metabolic phenotype in basal state by upregulating both the oxidative phosphorylation and the glycolytic pathway. We further revealed an increased compensatory glycolytic rate of PBMC and CD4+ T cells of ERU cases under mitochondrial stress conditions. These findings are in line with metabolic alterations of immune cells in other autoimmune diseases and basic research, where it was shown that activated immune cells have an increased need of energy and molecule demand for their effector function. We demonstrated a clear difference in the metabolic phenotypes of PBMC and, more specifically, CD4+ T cells of ERU cases and controls. These findings are another important step in understanding the pathogenesis of ERU and figuratively, human autoimmune uveitis.

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“…The possible candidates for pars planitis antigens were specified in conducted experiments involving humans. Those include human lens protein fraction (Doycheva et al 2007 ), HNK-1 carbohydrate epitope (Uusitalo et al 2000 ) and beta B1-crystallin (Stempel et al 2003 ).…”

Section: Pathogenesismentioning

confidence: 99%

Immunopathogenic Background of Pars Planitis

Przeździecka-Dołyk

Węgrzyn

Turno-Kręcicka

et al. 2015

Arch. Immunol. Ther. Exp.

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Pars planitis is defined as an intermediate uveitis of unknown background of systemic disease with characteristic formations such as vitreous snowballs, snowbanks and changes in peripheral retina. The incidence of pars planitis varies 2.4–15.4 % of the uveitis patients. The pathogenesis of the disease is to be determined in future. Clinical and histopathological findings suggest an autoimmune etiology, most likely as a reaction to endogenous antigen of unknown source, with T cells predominant in both vitreous and pars plana infiltrations. T cells subsets play an important role as a memory-effector peripheral cell. Snowbanks are formed as an effect of post inflammatory glial proliferation of fibrous astrocytes. There is also a genetic predisposition for pars planitis by human leukocyte antigen and several other genes. A coexistence of multiple sclerosis and optic neuritis has been described in numerous studies. Epiretinal membrane, cataract, cystoid macular edema, retinal detachment, retinal vasculitis, neovascularization, vitreous peripheral traction, peripheral hole formation, vitreous hemorrhage, disc edema are common complications observed in pars planitis. There is a need to expand the knowledge of the pathogenic and immunologic background of the pars planitis to create an accurate pharmacological treatment.

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High incidence of antibodies to lens proteins in sera from patients with uveitis

Cited by 5 publications

References 39 publications

Potential Sources and Roles of Adaptive Immunity in Age-Related Macular Degeneration: Shall We Rename AMD into Autoimmune Macular Disease?

Potential Sources and Roles of Adaptive Immunity in Age-Related Macular Degeneration: Shall We Rename AMD into Autoimmune Macular Disease?

Altered Metabolic Phenotype of Immune Cells in a Spontaneous Autoimmune Uveitis Model

Immunopathogenic Background of Pars Planitis

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