ABSTRACT
In order to satisfy the social and medical demands for optometric talents, the education model combining "medicine, teaching, research and prevention" was established, fully integrated with various resources like talents, facilities, equipment from the affiliated eye hospital, institute of ophthalmology and prevention and treatment center for juvenile myopia. Cultivation of high-quality applicative talents which integrated "knowledge, skills and accomplishment" were taken as the main line, Cultivation goal was established in accordance with requirement of talent. The curriculum system was optimized on the basis of competence. The teaching mode was reformed to "2+2" mode, "double-position teachers" became the requirement for the teaching staff and professional education comprehensive practice platform of "one entity, two wings" was constructed, with good effectiveness being achieved.
ABSTRACT
In order to satisfy the social and medical demands for optometric talents, the education model combining "medicine, teaching, research and prevention" was established, fully integrated with various resources like talents , facilities , equipment from the affiliated eye hospital , institute of ophthalmology and prevention and treatment center for juvenile myopia . Cultivation of high-quality applicative talents which integrated "knowledge, skills and accomplishment" were taken as the main line, Cultivation goal was established in accordance with requirement of talent . The curriculum system was optimized on the basis of competence. The teaching mode was reformed to "2+2" mode, "double-position teachers" became the requirement for the teaching staff and professional education comprehensive practice platform of"one entity, two wings"was constructed, with good effectiveness being achieved.
ABSTRACT
Background Previous studies showed that the pathogenesis of uveitis is related to γδ T cells.However,it remains unclear that how these cells are involved in experimental autoimmune uveitis (EAU).Objective This study aimed to observe the dynamic changes of γδ T cells in EAU and explore the role of γδ T cells in the pathological process of EAU.Methods Forty-five C57BL/6(B6) mice were assigned to the normal control group (six mice) and EAU model group (thirty-nine mice).The mice were immunized subcutaneously at 6 spots on the footpads,tail base,and flank with emulsion containing human interphotoreceptor retinoid binding protein1-20 (IRBP1-20) emulsified in complete Freund's adjuvant.After immunization,the mice were examined for clinical signs of EAU by using a Genesis-D camera.The changes of histopathology were compared by hematoxylin and eosin staining.Mouse lymphocytes were isolated and purified from the spleens of IRBP1-20-immunized or normal B6 mice by using a γδ T-cell isolation kit.Flow cytometry was used to detect the changes of intracellular expression of interleukin-17A (IL-17A),and then transferred the activated γδ T cells into EAU models to analyze the changes of clinical signs and histopathology of EAU.Experimental study program as well as the use and feeding of the animals were authorized by the Animal Management and Use Committee of Shandong Traditional Chinese Medicine University.Results The inflammatory symptoms in mouse eyes appeared on day 12 after modeling.The initial changes were fundal blood vessel thickening and minimal inflammatory cell infiltration.Then,multifocal chorioretinal lesions,serious vasculitis and linear lesions were observed on days 16-20,along with abundant lymphocyte infiltration in the vitreous and retinal disorganization.The inflammation symptom scores and the pathological inflammation scores at different time points after modeling had statistically significant differences (F =51.399,P =0.000;F =47.342,P =0.000).The inflammatory symptoms in the eyes began to abate from day 28 onwards.The number of γδ T cells was obviously increased during the inflammation phase of EAU at day 16-20 after modeling,with the number of γδ T cells was (5.67 ±-0.49) ％ and (5.78 ±±0.55) ％,respectively,which was significantly higher than (1.53 ± 0.14) ％ before modeling,with significant differences between them (both at P＜0.05),meanwhile CD69 levels and the integrin lymphocyte function-associated antigen-1 (LFA-1) and secreted IL-17A were elavated.The secretion level of IL-17A was (13.40±0.50)％ and (17.80±2.37)％ on day 16 and day 20 after modeling,respectively,which was significantly higher than (1.53 ± 0.19) ％ before modeling,with significant differences between them (P =0.000,0.001).The activated γδ T cells were transferred into EAU model,the inflammation symptom scores were 1.00 (1.00,2.00) after activated γδ T cells were transferred into EAU model,which was significantly higher than 0.75 (0.05,1.00) of the untransferred group (Z =27.00,P =0.03),and the symptoms of EAU were aggravated.Conclusions The proportion of γδ T cells reaches peak in inflammation of EAU,and the cells are activated.The activated γδ T cells in the EAU model play a immune regulation role by secreting IL-17A.
ABSTRACT
Background Studies show that regulatory T cells (Treg) are a kind of T cell subsets to negatively regulate immune response,and play an important role in maintaining immune homeostasis and immune tolerance.Autoimmune uveitis is an autoimmune disease,the regulation of Treg cells in pathogenesis and progression of autoimmune uveitis is not fully unelucidated.Objective This study was to observe the dynamic changes of Treg in experimental autoimmune uveitis (EAU) rats and explore the role of Treg cells in the pathological process of EAUrats.Methods Eighty four 6-8 week-old SPF Lewis rats were randomly divided into model group and control group.The mixed emulsifier of interphotoreceptor retinoid-binding protein (IRBP)1177-1191,tuberculin (TB),complete Freund adjuvant (CFA) and PBS (300 μl) was subcutaneously injected in double rear foot pad,abdominal side and back,and only equal amount of TB,CFA and PBS emulsifier was used in the same way in the control group.Ocular inflammation symptoms was examined at 9,13,18,23,28,35 and 48 days after modeling and scored based on the severity of the inflammatory.Six rats of each group were sacrificed in above time points respectively for the histopathological examination of iris,ciliary body and retinas by haematoxylin-eosin staining.The lymphocytes were isolated and cultured from rat spleens,and the proportion of Foxp3-labelled cells,a specific marker of Treg cells,was assayed by flow cytometry.The relative expression level of Foxp3 mRNA in the lymphocytes detected by using realtime quantitative PCR (RT-PCR).The use and care of the rats complied with the ARVO Statement.Results Eye inflammatory response appeared at 8 days after immunization,showing vasodilation and hyperemia of rat iris in the model group,and the response peaked at 13 days,with exudation and hypopyon in the anterior chamber.The highest inflammatory scores were 3.75±0.42 at day 13,and the ocular inflammation reaction was gradually relieved after that and disappeared at 23 days after immunity.A significant difference in ocular inflammatory scores of model rats was found among different time points (F =81.709,P ＜ 0.001);while no inflammatory symptom was observed in the control group.Histopathology examination showed obvious infiltration of inflammatory cells in the iris,ciliary body and retinas in model rats,including neutrophils,lymphocytes and mononuclear cells.The proportion of Foxp3-labelled cells in spleen lymphocytes was (5.50 ± 0.64)％,(13.36 ± 0.98)％,(10.34 ± 0.79)％,(9.58 ± 1.02)％,(6.73 ±0.81)％ and (5.58 ± 0.47) ％ in the model group on day 13,18,23,28,35,48 respectively,with statistically significant differences in comparison with (2.80 ± 0.38) ％,(3.36 ± 0.53) ％,(3.65 ± 0.57) ％,(3.37 ± 0.43) ％,(3.33±0.50)％ and (3.13±0.61)％ in the control group (t=-6.272,-15.556,-11.910,-9.753,-6.154,-5.491,all at P＜0.01).The change trend of Foxp3 mRNA expression was consistent to the dynamic change of the proportion of Foxp3-labelled cells.Conclusions The pathogenesis and development is closely associated with the dynamic changes of CD4+ CD25 + Foxp3+ Treg cells in EAU rats.