Objective To investigate the expression and significance of T-bet in experimental autoimmune uveoretinitis (EAU). Methods EAU was induced in 24 Lewis rats by immunization with retinal S-antigen (50 ?g) and complete Freund′s adjuvant, and another 4 rats were the healthy control. The rats with EAU were executed 7, 12, 15, 21 days after immunization, respectively. Immunohistochemical single and double staining were performed using monoclonal antibodies of T-bet or CD4 on the ocular wholemounts and the consecutive sections of the eye and spleen from both 24 immunized Lewis rats and 4 normal controls. The positive cells were counted under the optic microscope and the data were analyzed by SPSS 11.0 statistic software. Results A few T-bet positive cells were observed in the normal ocular tissues and spleen. The expressions of T-bet in the iris, retina, and spleen increased 7 days after immunization, reached the peak at the 15th day, and decreased at the 21st day, which were higher than those in the control. Double staining on the consecutive sections revealed that most of the T-bet positive cells were positive for CD4 monoclonal antibody. Conclusion T-bet may affect the occurrence of EAU by activating Th1 cells.

Objective To investigate the expression of T cell receptor (TCR) V ?8.3 gene on CD4+ T lymphocytes in the rats with experimental autoimmune uveoretinitis (EAU). Methods Eighteen Lewis rats were divided into EAU, complete Freund′s adjuvant, and the control group. Interphotoreceptor retinoid-binding protein (IRBP) R16 peptide was synthesized using Fmoc procedure for induction of EAU. Magnetic absorption cell sorting (MACS) method was used to isolate the CD4+ T lymphocytes from the spleen of the rats. Flow cytometry was used to monitor the efficiency of isolation. The expression of TCR V ?8.3 gene segment on CD4+T lymphocytes was determined by fluorescent quantitative polymerase chain reaction. Results EAU was successfully induced in the Lewis rats immunized with IRBP R16 peptide. The proportion of CD4+ T lymphocytes isolated by means of MACS was statistically higher than that before isolation (P

Objective To detect the expression and the function of Fractalkine( CX3CL1) and its receptor CX3CR1 in neurodegenerative changes of the retina.Methods Twelve 5XFAD mouse and twelve wild type mouse were enrolled. Frozen sections were prepared for histopathological tests.Immunofluorescence study for Amyloid β, CX3CL1 and CX3CR1 was carried out.Co-expression study for CX3CR1/CD11b or CX3CR1/CD68 was carried out.Total protein and total mRNA from the eyes of both 5XFAD and wild type mouse were extracted.The expression of mRNA and protein of CX3CL1 and CX3CR1 in the eyes were determined by reverse transcription-polymerase chain reaction ( RT-PCR) and Western blots test, respectively.Results In wild type mouse, both CX3CL1 and its receptor CX3CR1 can be detected in the retina with low expression, however there is no Amyloid βdepositions in retina.In 6 months 5XFAD mouse, an obvious up-regulated Amyloidβexpression can be seen in the RPE cells, and the number of both CX3CL1 and CX3CR1 positive cells has up-regulated in the ganglion cell layer of eyes accompanied with the increased expression of their mRNA and protein.The co-expression study showed that CX3CR1 co-expressed with CD11b, but not with CD68.Conclusion Fractalkine and its receptor play a role in Amyloid βinducing degenerative retinal inflammation in 5XFAD mouse.

Subretinal fibrosis(SRF),the end pathological stage of neovascular age-related macular degeneration(nAMD),can cause severe and irreversible vision loss in patients.In recent years,the high clinical incidence of SRF and the severe visual impairment it causes have led to a rapid development of SRF-related research.In order to systematically understand the clinical progress of SRF,recent studies on SRF secondary to nAMD were reviewed in this article.