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Assessment of the innate and adaptive immune system in proliferative vitreoretinopathy.

Zhang W, Tan J, Liu Y, Li W, Gao Q, Lehmann PV - Eye (Lond) (2012)

Bottom Line: Additionally, immunofluorescence analysis was performed.Carboxyfluorescein diacetate succinimidyl ester-labeled T cells that are specific for ovalbumin were detected in the inflamed vitreous and retina showing that T cells that are not specific for autoantigens present in the eye can migrate to PVR lesions.This study suggests that T- and B-cell immunity is not essential for the induction of PVR.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Case Western Reserve University, Cleveland, OH, USA.

ABSTRACT

Purpose: Proliferative vitreoretinopathy (PVR) is the leading cause of failure of surgery for rhegmatogenous retinal detachment. Although indirect evidence suggests that this disease might be autoimmune in nature, direct proof for this hypothesis is lacking. The purpose of this study was to determine in a murine model whether PVR can develop in the absence of T- or B-cell immunity.

Methods: Four- to six-week-old Rag-1 gene knockout (KO) and congenic wild-type mice (WT) on the C57.Bl/6 background were studied. PVR was induced by intravitreal injection of 3 μl dispase at the concentration of 0.2 U/μl. PVR development was monitored by electroretinograms, the macroscopic observation of hemorrhage, cataract, retinal folds, and of an uneven iris, as well as the histological detection of epiretinal membranes on haematoxylin-eosin stained tissue. Additionally, immunofluorescence analysis was performed. These manifestations of PVR were assessed 1, 2, 4, 6, and 8 weeks after the intravitreal injection.

Results: The data showed that the immune-deficient Rag-1 KO mice developed PVR with similar kinetics and severity as did the fully immune competent congenic WT mice. Carboxyfluorescein diacetate succinimidyl ester-labeled T cells that are specific for ovalbumin were detected in the inflamed vitreous and retina showing that T cells that are not specific for autoantigens present in the eye can migrate to PVR lesions. Therefore, the mere presence of T cells in PVR lesions does not imply an autoimmune pathogenesis.

Conclusion: This study suggests that T- and B-cell immunity is not essential for the induction of PVR.

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Related in: MedlinePlus

Early inflammatory infiltration occurred at the same speed in WT and KO mice. (a) H&E staining of the retina after dispase or saline injection. (b) H&E staining of the aqueous angle. Arrows indicate neutrophils. (c) Immunofluorescence analysis showing the absence of T cells (CD3+), macrophages (F4/80+), and NK cells (CD56+) 48 h after dispase injection.
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fig3: Early inflammatory infiltration occurred at the same speed in WT and KO mice. (a) H&E staining of the retina after dispase or saline injection. (b) H&E staining of the aqueous angle. Arrows indicate neutrophils. (c) Immunofluorescence analysis showing the absence of T cells (CD3+), macrophages (F4/80+), and NK cells (CD56+) 48 h after dispase injection.

Mentions: We harvested eyes from KO and WT mice that were untreated, or 4, 8, 12, 24, and 48 h and 5 days after injection of 3 μl of dispase. The eyes of control mice were injected with 3 μl saline, and studied at these time points. HE staining showed that polymorphonuclear neutrophils were the main infiltrating cell type in the eyes of dispase-injected KO and WT mice. In both strains, the neutrophils started to appear 8 h post injection, peaked at 24–48 h, and decreased by day 5 (Figure 3). In contrast, eyes of the saline-injected KO or WT mice did not show an infiltrate at any of these time points.


Assessment of the innate and adaptive immune system in proliferative vitreoretinopathy.

Zhang W, Tan J, Liu Y, Li W, Gao Q, Lehmann PV - Eye (Lond) (2012)

Early inflammatory infiltration occurred at the same speed in WT and KO mice. (a) H&E staining of the retina after dispase or saline injection. (b) H&E staining of the aqueous angle. Arrows indicate neutrophils. (c) Immunofluorescence analysis showing the absence of T cells (CD3+), macrophages (F4/80+), and NK cells (CD56+) 48 h after dispase injection.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3376296&req=5

fig3: Early inflammatory infiltration occurred at the same speed in WT and KO mice. (a) H&E staining of the retina after dispase or saline injection. (b) H&E staining of the aqueous angle. Arrows indicate neutrophils. (c) Immunofluorescence analysis showing the absence of T cells (CD3+), macrophages (F4/80+), and NK cells (CD56+) 48 h after dispase injection.
Mentions: We harvested eyes from KO and WT mice that were untreated, or 4, 8, 12, 24, and 48 h and 5 days after injection of 3 μl of dispase. The eyes of control mice were injected with 3 μl saline, and studied at these time points. HE staining showed that polymorphonuclear neutrophils were the main infiltrating cell type in the eyes of dispase-injected KO and WT mice. In both strains, the neutrophils started to appear 8 h post injection, peaked at 24–48 h, and decreased by day 5 (Figure 3). In contrast, eyes of the saline-injected KO or WT mice did not show an infiltrate at any of these time points.

Bottom Line: Additionally, immunofluorescence analysis was performed.Carboxyfluorescein diacetate succinimidyl ester-labeled T cells that are specific for ovalbumin were detected in the inflamed vitreous and retina showing that T cells that are not specific for autoantigens present in the eye can migrate to PVR lesions.This study suggests that T- and B-cell immunity is not essential for the induction of PVR.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Case Western Reserve University, Cleveland, OH, USA.

ABSTRACT

Purpose: Proliferative vitreoretinopathy (PVR) is the leading cause of failure of surgery for rhegmatogenous retinal detachment. Although indirect evidence suggests that this disease might be autoimmune in nature, direct proof for this hypothesis is lacking. The purpose of this study was to determine in a murine model whether PVR can develop in the absence of T- or B-cell immunity.

Methods: Four- to six-week-old Rag-1 gene knockout (KO) and congenic wild-type mice (WT) on the C57.Bl/6 background were studied. PVR was induced by intravitreal injection of 3 μl dispase at the concentration of 0.2 U/μl. PVR development was monitored by electroretinograms, the macroscopic observation of hemorrhage, cataract, retinal folds, and of an uneven iris, as well as the histological detection of epiretinal membranes on haematoxylin-eosin stained tissue. Additionally, immunofluorescence analysis was performed. These manifestations of PVR were assessed 1, 2, 4, 6, and 8 weeks after the intravitreal injection.

Results: The data showed that the immune-deficient Rag-1 KO mice developed PVR with similar kinetics and severity as did the fully immune competent congenic WT mice. Carboxyfluorescein diacetate succinimidyl ester-labeled T cells that are specific for ovalbumin were detected in the inflamed vitreous and retina showing that T cells that are not specific for autoantigens present in the eye can migrate to PVR lesions. Therefore, the mere presence of T cells in PVR lesions does not imply an autoimmune pathogenesis.

Conclusion: This study suggests that T- and B-cell immunity is not essential for the induction of PVR.

Show MeSH
Related in: MedlinePlus