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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

Development of clinical PVR in Rag-1 KO and WT mice after dispase injection. A total of 10 mice in each group were injected intraocularly with 0.2 U/μl dispase. At the time points specified, the eyes were examined for: (a) macroscopic presentation of PVR symptoms; and (b) histological evidence for PVR as established on H&E-stained sections. (c) Skot ERGs recording α- and β-wave amplitudes. The contralateral untreated eyes were used as controls. The data in both panels represent the cumulative results obtained on 25 Rag-1 KO mice after dispase injection.
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fig2: Development of clinical PVR in Rag-1 KO and WT mice after dispase injection. A total of 10 mice in each group were injected intraocularly with 0.2 U/μl dispase. At the time points specified, the eyes were examined for: (a) macroscopic presentation of PVR symptoms; and (b) histological evidence for PVR as established on H&E-stained sections. (c) Skot ERGs recording α- and β-wave amplitudes. The contralateral untreated eyes were used as controls. The data in both panels represent the cumulative results obtained on 25 Rag-1 KO mice after dispase injection.

Mentions: The rate at which PVR developed after dispase injection was monitored in Rag-1 KO and WT mouse strains to assess the severity and kinetics of PVR development in the absence or presence of a functional adaptive immune system. In both type of mice, the macroscopic signs of the disease developed in parallel. In both the groups, the first signs of PVR appeared 2 weeks after dispase injection, affecting about 25% of the mice (Figure 2a). The percentages of PVR-positive mice gradually increased in the subsequent weeks reaching about 70% for both the groups by 8th week. Statistical analysis showed no significant difference between the Rag KO and the WT group at weeks 2, 4, 6, and 8 with P-values of 0.2163, 0.2503, 0.2176, and 0.2642, respectively.


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)

Development of clinical PVR in Rag-1 KO and WT mice after dispase injection. A total of 10 mice in each group were injected intraocularly with 0.2 U/μl dispase. At the time points specified, the eyes were examined for: (a) macroscopic presentation of PVR symptoms; and (b) histological evidence for PVR as established on H&E-stained sections. (c) Skot ERGs recording α- and β-wave amplitudes. The contralateral untreated eyes were used as controls. The data in both panels represent the cumulative results obtained on 25 Rag-1 KO mice after dispase injection.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Development of clinical PVR in Rag-1 KO and WT mice after dispase injection. A total of 10 mice in each group were injected intraocularly with 0.2 U/μl dispase. At the time points specified, the eyes were examined for: (a) macroscopic presentation of PVR symptoms; and (b) histological evidence for PVR as established on H&E-stained sections. (c) Skot ERGs recording α- and β-wave amplitudes. The contralateral untreated eyes were used as controls. The data in both panels represent the cumulative results obtained on 25 Rag-1 KO mice after dispase injection.
Mentions: The rate at which PVR developed after dispase injection was monitored in Rag-1 KO and WT mouse strains to assess the severity and kinetics of PVR development in the absence or presence of a functional adaptive immune system. In both type of mice, the macroscopic signs of the disease developed in parallel. In both the groups, the first signs of PVR appeared 2 weeks after dispase injection, affecting about 25% of the mice (Figure 2a). The percentages of PVR-positive mice gradually increased in the subsequent weeks reaching about 70% for both the groups by 8th week. Statistical analysis showed no significant difference between the Rag KO and the WT group at weeks 2, 4, 6, and 8 with P-values of 0.2163, 0.2503, 0.2176, and 0.2642, respectively.

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