Interphotoreceptor retinoid-binding protein (IRBP)-deficient C57BL/6 mice have enhanced immunological and immunopathogenic responses to IRBP and an altered recognition of IRBP epitopes

Avichezer, Dody; Liou, Gregory I.; Chan, Chi Chao; Lewis, Giavonni; Wiggert, Barbara; Donoso, Larry A.; Nickerson, John M.; Crawford, M; Caspi, Rachel R

doi:10.1016/j.jaut.2003.08.004

Cited by 24 publications

(21 citation statements)

References 31 publications

(61 reference statements)

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“…The clinical scores and histopathologic scores were showed in Tables S1 and S2, according to the previous description. [37][38][39][40] 2.2 | CD83 + CCR7 + NK or CD83 -CCR7 -NK cell adoptive transfers…”

Section: Experimental Autoimmune Uveitismentioning

confidence: 99%

CD83⁺CCR7⁺ NK cells induced by interleukin 18 by dendritic cells promote experimental autoimmune uveitis

Man

Wang

et al. 2018

J Cellular Molecular Medi

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Natural killer (NK) cells have been reported to play a pathological role in autoimmune uveitis. However, the mechanisms regarding NK cells in uveitis and factors that affect NK‐cell activation in this condition remain unclear. Here, we report that the number of CD3 ‐ NK1.1 + CD83 + CCR7 + cells is increased in the inflamed eyes within a mouse model of experimental autoimmune uveitis (EAU), and these cells express elevated levels of NKG2D, CD69 and IFN‐γ. Adoptively transferring CD83 + CCR7 + NK cells aggravates EAU symptoms and increases the number of CD4 + IFN‐γ + T cells and dendritic cells (DCs) within the eye. These CD83 + CCR7 + NK cells then promote the maturation of DCs and IFN‐γ expression within T cells as demonstrated in vitro. Furthermore, IL‐18, as primarily secreted by DCs in the eyes, is detected to induce CD83 + CCR7 + NK cells. In EAU mice, anti‐IL‐18R antibody treatment also decreases retinal tissue damage, as well as the number of infiltrating CD83 + CCR7 + NK cells, T cells and DCs in the inflamed eyes and spleens of EAU mice. These results suggest that CD83 + CCR7 + NK cells, as induced by IL‐18 that primarily secreted by DCs, play a critical pathological role in EAU. Anti‐IL‐18R antibody might serve as a potential therapeutic agent for uveitis through its capacity to inhibit CD83 + CCR7 + NK cells infiltration.

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Section: Experimental Autoimmune Uveitismentioning

confidence: 99%

CD83⁺CCR7⁺ NK cells induced by interleukin 18 by dendritic cells promote experimental autoimmune uveitis

Man

Wang

et al. 2018

J Cellular Molecular Medi

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“…To further characterize these CD8 ϩ autoreactive T cells and determine their role in the pathogenesis of mouse EAU, we immunized B6 mice with IRBP1-20, a known uveitogenic peptide derived from IRBP (3,18), then prepared T cells from these mice at day 13 p.i. and labeled them with CFSE before stimulation with IRBP1-20 in the presence of irradiated syngeneic APCs (spleen cells).…”

Section: Detection Of Cd8 ϩ Irbp1-20-specific T Cells Using Cfse Staimentioning

confidence: 99%

A Shared Epitope of the Interphotoreceptor Retinoid-Binding Protein Recognized by the CD4+ and CD8+ Autoreactive T Cells

Shao

Peng

Liao

et al. 2005

The Journal of Immunology

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We previously demonstrated that cultures of rat uveitogenic T cells rapidly become dominated by CD4+ cells, but activation of CD8+ autoreactive T cells also occurred during the in vitro culture of in vivo-primed T cells. In the present study, we show that the commonly used uveitogenic peptide, interphotoreceptor retinoid-binding protein (IRBP) 1–20, generated both CD4+ and CD8+ autoreactive T cells in the C57BL/6 (B6) mouse and that this 20-mer contains at least two distinct antigenic epitopes. To determine whether the CD8 response was Ag-specific and whether CD4+ and CD8+ IRBP1–20-specific T cells recognize distinct antigenic epitopes, we prepared highly purified CD4+ and CD8+ T cells from IRBP1–20-primed mice and tested their proliferative response to a large panel of truncated peptides derived from IRBP1–20. The results showed that both CD4+ and CD8+ T cells recognized the same spectrum of peptides. In addition, peptides P10–18 were found to bind effectively to CD8+ IRBP1–20-specific T cells when complexed with recombinant H-2Kb and also stimulate the proliferation and cytokine production of CD4+ IRBP1–20-specific T cells. Our results document for the first time that CD8+ and CD4+ autoreactive T cells display characteristic epitope recognition and they both recognize the same core epitope.

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“…These phenomena can be related to interstrain differences in their genetic background [3]. For example, B6 mice are more susceptible than BALB/c mice to induction of experimental, organ-specific autoimmune diseases, such as experimental autoimmune myasthenia gravis [4] and experimental autoimmune uveitis [5][6][7]. In contrast with B6 mice, BALB/c mice display increased susceptibility to tumorigenesis, including mammary [8,9] and colon tumors [10].…”

Section: Introductionmentioning

confidence: 99%

BALB/c mice have more CD4+CD25+ T regulatory cells and show greater susceptibility to suppression of their CD4+CD25− responder T cells than C57BL/6 mice

Chen

Oppenheim

Howard

2005

Journal of Leukocyte Biology

111

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Increasing evidence indicates that CD4(+)CD25(+) T regulatory (Treg) cells control a wide spectrum of immune responses. The initial identification of CD4(+)CD25(+) Treg cell as a "professional suppressor" was based on observations made in BALB/c mice. This mouse strain is well known to preferentially develop T helper cell type 2 responses, to be more susceptible to intracellular parasite infection, to have a higher tumor incidence, and to be more resistant to the induction of autoimmune diseases, as compared with C57BL/6 (B6) mice. We therefore decided to compare Treg cell function of B6 and BALB/c mice. We observed that the frequency of CD4(+)CD25(+) T cells in the thymus and peripheral lymphoid organs of BALB/c mice was higher than in B6 mice. CD4(+)CD25(+) Treg cells from both mouse strains shared similar phenotypic properties, including expression of characteristic immunological markers and hyporesponsiveness to T cell receptor cross-linking and in their capacity to suppress proliferation of BALB/c CD4(+)CD25(-) T responder (Tres) cells. However, CD4(+)CD25(-) Tres cells from B6 mice were notably less susceptible to suppression by CD4(+)CD25(+) Treg cells from either mouse strain. Our data suggest that the number and the level of suppression of CD4(+)CD25(+) Treg cells for CD4(+)CD25(-) Tres cells may be dictated by genetic background. Our data also suggest that differences in the CD4(+)CD25(+) Treg cell number and the susceptibility of CD4(+)CD25(-) Tres cells may, at least in part, account for the differences in immune response between B6 and BALB/c strains of mice.

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Interphotoreceptor retinoid-binding protein (IRBP)-deficient C57BL/6 mice have enhanced immunological and immunopathogenic responses to IRBP and an altered recognition of IRBP epitopes

Cited by 24 publications

References 31 publications

CD83⁺CCR7⁺ NK cells induced by interleukin 18 by dendritic cells promote experimental autoimmune uveitis

CD83⁺CCR7⁺ NK cells induced by interleukin 18 by dendritic cells promote experimental autoimmune uveitis

A Shared Epitope of the Interphotoreceptor Retinoid-Binding Protein Recognized by the CD4+ and CD8+ Autoreactive T Cells

BALB/c mice have more CD4+CD25+ T regulatory cells and show greater susceptibility to suppression of their CD4+CD25− responder T cells than C57BL/6 mice

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Interphotoreceptor retinoid-binding protein (IRBP)-deficient C57BL/6 mice have enhanced immunological and immunopathogenic responses to IRBP and an altered recognition of IRBP epitopes

Cited by 24 publications

References 31 publications

CD83+CCR7+ NK cells induced by interleukin 18 by dendritic cells promote experimental autoimmune uveitis

CD83+CCR7+ NK cells induced by interleukin 18 by dendritic cells promote experimental autoimmune uveitis

A Shared Epitope of the Interphotoreceptor Retinoid-Binding Protein Recognized by the CD4+ and CD8+ Autoreactive T Cells

BALB/c mice have more CD4+CD25+ T regulatory cells and show greater susceptibility to suppression of their CD4+CD25− responder T cells than C57BL/6 mice

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CD83⁺CCR7⁺ NK cells induced by interleukin 18 by dendritic cells promote experimental autoimmune uveitis

CD83⁺CCR7⁺ NK cells induced by interleukin 18 by dendritic cells promote experimental autoimmune uveitis