Rat T-cell lines specific to a nonimmunodominant determinant of a retinal protein (IRBP) produce uveoretinitis and pinealitis

Hu, Lihong; Redmond, T. Michael; Sanui, H; Kuwabara, Toichiro; McAllister, Cathy G.; Wiggert, Barbara; Chader, Gerald J.; Gery, Igal

doi:10.1016/0008-8749(89)90165-2

Cited by 32 publications

(14 citation statements)

References 29 publications

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“…The recurrent nature of autoimmune uveitis may result in severe clinical complications, such as cystoid macular edema, cataract formation, and glaucoma, even though a single episode of the disease usually does not cause permanent visual loss. Experimental autoimmune uveitis (EAU) 3 can be elicited in rodents following immunization with several different Ags, e.g., retinal-soluble Ag, interphotoreceptor retinal-binding protein (IRBP) (1, 2), melanin-associated Ag (MAA) (3,4), and myelin proteins (5-7), as well as by the adoptive transfer of uveitogenic T cells between syngeneic rodents (7)(8)(9)(10). Uveitogenic T cells that mediate EAU are assumed to be exclusively CD4 ϩ T cells.…”

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confidence: 99%

Conversion of Monophasic to Recurrent Autoimmune Disease by Autoreactive T Cell Subsets

Shao

Song

Sun

et al. 2003

The Journal of Immunology

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Autoimmune uveitis has been elicited in susceptible rodents by several ocular-specific Ags. In most of these animal models the induced uveitis is acute and monophasic. Because recurrent uveitis poses the highest risk for blinding ocular complications in human disease, a spontaneous relapsing animal model would be most helpful in understanding the disease pathogenesis. In our current study we have observed that the adoptive transfer of interphotoreceptor retinoid-binding protein residues 1177–1191-specific T cells to naive Lewis rats induced a chronic relapsing disease, in contrast to the monophasic disease induced by immunization with interphotoreceptor retinoid-binding protein residues 1177–1191 emulsified in CFA. The chronic relapsing uveitis induced by autoreactive T cell subsets is dependent on the number of autoreactive T cells generated as well as their activation status. Our study documented a spontaneous model of recurrent uveitis in the rat, which should assist us in the study of disease pathogenesis and the design of specific therapy.

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confidence: 99%

Conversion of Monophasic to Recurrent Autoimmune Disease by Autoreactive T Cell Subsets

Shao

Song

Sun

et al. 2003

The Journal of Immunology

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“…Although a single episode of the disease usually does not cause permanent visual loss, the recurrent nature of uveitis can result in severe clinical complications, such as cystoid macular edema, cataract formation, and glaucoma. Experimental autoimmune uveitis (EAU) 3 can be elicited in rodents by immunization with several different Ags, such as surface Ag (SAg), interphotoreceptor retinal-binding protein (IRBP) (1, 2), melanin-associated Ag (3,4), or myelin proteins (5-7), or by the adoptive transfer of uveitogenic T cells between syngeneic rodents (7)(8)(9)(10). These uveitogenic T cells are assumed to be exclusively CD4 ϩ T cells.…”

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confidence: 99%

Characterization of Rat CD8+ Uveitogenic T Cells Specific for Interphotoreceptor Retinal-Binding Protein 1177–1191

Shao

Sun

Kaplan

et al. 2004

The Journal of Immunology

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The uveitogenic T cells that mediate experimental autoimmune uveitis are commonly assumed to be exclusively CD4+. In the present study, we showed that, although a panel of long-term cultured rat uveitogenic T cell lines specific for the interphotoreceptor retinal-binding protein peptide, R16, all expressed CD4, ∼40% of the R16-specific uveitogenic T cells freshly prepared from Ag-immunized rats were CD8+αβTCR+, as demonstrated by CFSE staining. We showed that the expansion of these CD8+αβTCR+ T cells was Ag-specific and that highly purified CD8+ R16-specific T cells were able to induce uveitis on transfusion into naive rats. Moreover, CD8+ uveitogenic T cells more readily switched phenotype from, and to, TCR−CD8−CD4− during in vivo or in vitro activation compared with their CD4+ counterparts. In a previous study, we showed that highly purified CD8+ myelin oligodendrocyte glycoprotein-specific T cells induced more severe autoimmune encephalomyelitis than the corresponding CD4+ T cells. In this study, we show that an interphotoreceptor retinal-binding protein peptide consistently activated a high proportion of CD8+αβTCR+ T cells, which were uveitogenic in Lewis rats.

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“…The invading T cells are probably carrying the autoantigenic determinants as shown in other models of autoimmune disease such as experimental autoimmune encephalitis or autoimmune uveitis [25,26]. Once the autoimmune cascade is started, plasma cells were stimulated to secrete immunoglobulins which could be detected as autoantibodies at 30 and 42 kD in the membranous labyrinth group and 30 kD in the modiolus group.…”

Section: Discussionmentioning

confidence: 99%

A Rat T-Cell Line That Mediates Autoimmune Disease of the Inner Ear in the Lewis Rat

Gloddek

Gloddek²,

Arnold³

1999

ORL

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In various patterns of sensorineural hearing loss including Ménière’s disease, which may show improvement in auditory function following immunosuppressive therapy, an isolated autoimmune disease of the inner ear has been postulated. Because of the lack of well-defined diagnostic criteria to identify autoimmune processes within the inner ear and the fact that the human inner ear is one of the few organs of the body not amenable to diagnostic biopsy, there has been great interest in developing animal models that mimic these clinical entities. Previous studies have found evidence that this process might be cell mediated and that the endolymphatic sac functions as an immunodefensive organ for the inner ear. By heterologous immunization of inbred Lewis rats with inner ear tissue, an autoreactive inner-ear-specific T helper cell line was established. After passive transfer of these cells a labyrinthitis was induced in recipient animals. Immunohistochemically, T helper cells were first identified in the cochlea suggesting that this cell type might carry the autoantigenic epitope. Autoantibodies against inner ear tissue were demonstrated in animals with histologically evident labyrinthitis. We conclude that this experimental design can serve as an animal model for cell-mediated autoimmune disease of the inner ear and could be used to explain the etiology of certain types of sensorineural hearing loss such as Ménière’s disease. With this approach the identification of the causative autoantigen should be possible and will lead to the development of appropriate clinical tests to diagnose autoimmune diseases of the inner ear in humans.

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Rat T-cell lines specific to a nonimmunodominant determinant of a retinal protein (IRBP) produce uveoretinitis and pinealitis

Cited by 32 publications

References 29 publications

Conversion of Monophasic to Recurrent Autoimmune Disease by Autoreactive T Cell Subsets

Conversion of Monophasic to Recurrent Autoimmune Disease by Autoreactive T Cell Subsets

Characterization of Rat CD8+ Uveitogenic T Cells Specific for Interphotoreceptor Retinal-Binding Protein 1177–1191

A Rat T-Cell Line That Mediates Autoimmune Disease of the Inner Ear in the Lewis Rat

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