S antigen-induced experimental autoimmune uveo-retinitis in rats

Kozak, Y. de; Sakai, Jill A.; Thillaye, B.; Faure, Jean‐Pierre

doi:10.3109/02713688108998359

Cited by 173 publications

(49 citation statements)

References 10 publications

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“…The general BSCR pathogenic features are similar to those observed in S-antigen-induced experimental autoimmune uveoretinitis in monkey (29,30). S-antigen was also shown to be uveitogenic in rodent models (31)(32)(33)(34)(35)(36)(37).…”

Section: Resultsmentioning

confidence: 99%

Spontaneous retinopathy in HLA-A29 transgenic mice

Szpak

Vieville

Tabary

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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Humans who have inherited the class I major histocompatibility allele HLA-A29 have a markedly increased relative risk of developing the eye disease termed birdshot chorioretinopathy. This disease affecting adults is characterized by symmetrically scattered, small, cream-colored spots in the fundus associated with retinal vasculopathy and inflammatory signs causing damage to the ocular structures, leading regularly to visual loss. To investigate the role of HLA-A29 in this disease, we introduced the HLA-A29 gene into mice. Aging HLA-A29 transgenic mice spontaneously developed retinopathy, showing a striking resemblance to the HLA-A29-associated chorioretinopathy. These results strongly suggest that HLA-A29 is involved in the pathogenesis of this disease. Elucidation of the role of HLA-A29 should be assisted by this transgenic model.

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Section: Resultsmentioning

confidence: 99%

Spontaneous retinopathy in HLA-A29 transgenic mice

Szpak

Vieville

Tabary

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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“…EAU is a T cell-mediated autoimmune disease that can be induced in rodents by challenge with retinal antigen or its partial polypeptide [17,18] or by systemic administration of in vitro-activated T cells specific for a retinal antigen [19,20]. Disease is initiated as a result of sensitization of lymphocytes to retinal antigens, leading to the emigration of lymphocytes and macrophages, from the circulation into the neuroretina and structural damage to the retina [16].…”

Section: Introductionmentioning

confidence: 99%

Reduction in shear stress, activation of the endothelium, and leukocyte priming are all required for leukocyte passage across the blood—retina barrier

Xu¹,

Manivannan

Goatman

et al. 2003

Journal of Leukocyte Biology

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The passage of leukocytes across the blood-retina barrier at the early stages of an inflammatory reaction is influenced by a complex series of interactions about which little is known. In particular, the relationship between hydrodynamic factors, such as shear stress and leukocyte velocity, to the adherence and subsequent extravasation of leukocytes into the retina is unclear. We have used a physiological method, scanning laser ophthalmoscopy, to track labeled leukocytes circulating in the retina, followed by confocal microscopy of retinal flatmounts to detect infiltrating cells at the early stage of experimental autoimmune uveitis. This has shown that retinal vessels are subjected to high shear stress under normal circumstances. During the inflammatory reaction, shear stress in retinal veins is reduced 24 h before leukocyte infiltration. This reduction is negatively correlated with leukocyte rolling and sticking in veins and postcapillary venules, the sites of leukocyte extravasation. Activation of vascular endothelial cells is also a prerequisite for leukocyte rolling and infiltration. In addition, antigen priming of leukocytes is influential at the early stage of inflammation, and this is seen clearly in the reduction in rolling velocity and adherence of the primed leukocytes in activated retinal venules, 9 days postimmunization.

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“…Analogous to S100β, arrestin is also a calcium-binding protein that is found in the brain (β-arrestin) and retina (23)(24)(25). It is well known that MS is associated with intermediate uveitis (26)(27)(28) and arrestin can be used to induce experimental autoimmune uveoretinitis (EAU) (29)(30)(31). Autoantibodies to both brain and retina arrestin have been reported in MS patients (11,32,33), although the T-cell proliferative response to this antigen has not been reported.…”

Section: Introductionmentioning

confidence: 99%

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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S antigen-induced experimental autoimmune uveo-retinitis in rats

Cited by 173 publications

References 10 publications

Spontaneous retinopathy in HLA-A29 transgenic mice

Spontaneous retinopathy in HLA-A29 transgenic mice

Reduction in shear stress, activation of the endothelium, and leukocyte priming are all required for leukocyte passage across the blood—retina barrier

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

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