结节病是一种原因不明的多系统累及的肉芽肿性疾病,主要侵犯肺和淋巴系统,其次是眼部和皮肤.肉芽肿是最复杂的免疫反应之一,涉及多种细胞,且细胞分子间的相互作用随时间而动态变化.近年对结节病发病机制的新见解不断涌现,包括结节病的...结节病是一种原因不明的多系统累及的肉芽肿性疾病,主要侵犯肺和淋巴系统,其次是眼部和皮肤.肉芽肿是最复杂的免疫反应之一,涉及多种细胞,且细胞分子间的相互作用随时间而动态变化.近年对结节病发病机制的新见解不断涌现,包括结节病的先天免疫、Th17细胞、Treg细胞、血清淀粉样蛋白A(serum amyloid A protein,SAA)和其他因素的作用.展开更多
AIM:To investigate the feasibility and mechanism of immune tolerance in allergic conjunctivitis.METHODS:The allergic conjunctivitis immune tolerance mice model was established by ragweed pollen(RW)and the related cyto...AIM:To investigate the feasibility and mechanism of immune tolerance in allergic conjunctivitis.METHODS:The allergic conjunctivitis immune tolerance mice model was established by ragweed pollen(RW)and the related cytokines were detected.The mice were divided into 9 groups and the maslinic acid(MA)or PBS were given for different group after modeling.The expression levels of chemokine ligand 5(CCL5)and P-65 in the conjunctival tissue were analyzed by immunohistochemistry,quantitative reverse transcription polymerase chain reaction(q RT-PCR)and Western blot.The percentage of interleukin-17(IL-17)and CD4+CD25+in the splenocyte supernatant was analyzed by flow cytometry.Fur thermore,the serum and splenocyte supernatant concentration of total-IgE,interleukin-10(IL-10),and IL-17 was analyzed by enzyme linked immune response(ELISA).RESULTS:After the model was established,symptoms of conjunctivitis were alleviated,the level of P-65,CCL5,IL-17,and total-IgE was raised,while the expression of IL-10,CD4+CD25+was decreased.This result fully demonstrated that a typical IL-17/regulatory-T-cells(Treg cells)imbalance and NF-κB activation.When the NF-κB signal pathway was suppressed,it showed that there was a further relief of conjunctivitis in mice.At the same time,the expression of total-IgE,IL-17,and CCL5 was decreased and the expression of anti-inflammatory factor(IL-10,CD4+CD25+)was increased.CONCLUSION:In the state of immune tolerance,symptoms of conjunctivitis in mice are alleviated,the Th-17 cells of allergic conjunctivitis mice are inhibited,and Treg cells activity is enhanced.展开更多
文摘结节病是一种原因不明的多系统累及的肉芽肿性疾病,主要侵犯肺和淋巴系统,其次是眼部和皮肤.肉芽肿是最复杂的免疫反应之一,涉及多种细胞,且细胞分子间的相互作用随时间而动态变化.近年对结节病发病机制的新见解不断涌现,包括结节病的先天免疫、Th17细胞、Treg细胞、血清淀粉样蛋白A(serum amyloid A protein,SAA)和其他因素的作用.
基金Supported by the Provincial Innovation Team for Cataract and Ocular Fundus Disease in the Second People’s Hospital of Yunnan Province(No.2017HC010)the Key Laboratory of Yunnan Province for the Prevention and Treatment of Ophthalmology(No.2017DG008)Expert Workstation of Yao Ke(No.2017IC064)。
文摘AIM:To investigate the feasibility and mechanism of immune tolerance in allergic conjunctivitis.METHODS:The allergic conjunctivitis immune tolerance mice model was established by ragweed pollen(RW)and the related cytokines were detected.The mice were divided into 9 groups and the maslinic acid(MA)or PBS were given for different group after modeling.The expression levels of chemokine ligand 5(CCL5)and P-65 in the conjunctival tissue were analyzed by immunohistochemistry,quantitative reverse transcription polymerase chain reaction(q RT-PCR)and Western blot.The percentage of interleukin-17(IL-17)and CD4+CD25+in the splenocyte supernatant was analyzed by flow cytometry.Fur thermore,the serum and splenocyte supernatant concentration of total-IgE,interleukin-10(IL-10),and IL-17 was analyzed by enzyme linked immune response(ELISA).RESULTS:After the model was established,symptoms of conjunctivitis were alleviated,the level of P-65,CCL5,IL-17,and total-IgE was raised,while the expression of IL-10,CD4+CD25+was decreased.This result fully demonstrated that a typical IL-17/regulatory-T-cells(Treg cells)imbalance and NF-κB activation.When the NF-κB signal pathway was suppressed,it showed that there was a further relief of conjunctivitis in mice.At the same time,the expression of total-IgE,IL-17,and CCL5 was decreased and the expression of anti-inflammatory factor(IL-10,CD4+CD25+)was increased.CONCLUSION:In the state of immune tolerance,symptoms of conjunctivitis in mice are alleviated,the Th-17 cells of allergic conjunctivitis mice are inhibited,and Treg cells activity is enhanced.
