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91.
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目的探讨白细胞介素37b重组蛋白(rmIL-37b)通过调节CD39/ATP轴抑制树突状细胞(DC)诱导类风湿性关节炎(RA)大鼠炎症反应的机制。方法将SD大鼠随机分为空白对照组(CTL)、CIA模型组、rmIL-37b 5μg/kg组、rmIL-37b 10μg/kg组,每组各10只。除了空白对照组外,其余大鼠采用含有卡介苗的完全弗氏佐剂和牛Ⅱ型胶原混合乳液免疫刺激,建立CIA模型。确定建模成功当天(D0),rmIL-37b组分别尾静脉注射5μg/kg、10μg/kg rmIL-37b;CTL组和CIA模型组注射相同体积的(1 ml/kg)生理盐水,连续给药15 d。免疫组化法检测滑膜组织Nod样受体蛋白3(NRPL3)炎症小体的表达,流式细胞术检测DC表型,另外试剂盒检测血清三磷酸腺苷(ATP)和免疫学指标。结果与CIA模型组相比,rmIL-37b 10μg/kg组大鼠足容积、AI值、NLRP3炎症小体表达量、血清ATP、IL-1β、IL-18、肿瘤坏死因子α(TNF-α)、抗Ⅱ型胶原抗体亚型(anti-ColⅡ-IgG、anti-ColⅡ-IgG2a)水平均降低,同时DC表面CD... 相似文献
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Objective:To investigate the therapeutic effects of Qingre Quyu Granule(清热祛瘀颗粒,QQG)on the patients with severe carotid stenosis,and to explore the mechanism of it.Methods:Ninety-six patients with severe carotid stenosis were enrolled in the study and were classified into a QQG group(n=48) and a control group(n=48) randomly using consecutively numbered envelopes.The patients in the QQG group were given QQG and Western medicine,those in the control group were given Western medicine merely,the course of treatment was 16 weeks.All patients went through endarterectomy after treatment.Plaques were subjected to the analysis of CD3,CD68,soluble intercellular adhesion molecule 1(ICAM-1),matrix metalloprotease-9(MMP-9),CD40 L,tenascin-C,and collagen content lipid content by immunohistochemistry or polarized light analysis.Results:By the end of experiment,the expressions of CD3,CD68,ICAM-1,MMP9,CD40 L and tenascin-C on the plaques were statistically significant lower in the QQG group compared with the control group(P0.01).The lipid content of the plaque was also significantly lower in the QQG group compared with the control group(P0.01).The interstitial collagen in the tissue sections of the plaques was also significantly higher in the QQG group in comparison with the control group(P0.01).Conclusion:QQG could stabilize carotid artery plaques through inhibiting pro-inflammation factors and restraining the tenascin-C and MMP9 pathway. 相似文献
95.
Intralymphatic histiocytosis comprises M2 macrophages in superficial dermal lymphatics with or without smooth muscles 下载免费PDF全文
Noriki Fujimoto Gen Nakanishi Toshiaki Manabe Taku Fujimura Toshihiro Tanaka 《Journal of cutaneous pathology》2016,43(10):898-902
Intralymphatic histiocytosis represents a rare reactive disorder, which is characterized by the accumulation of macrophages within lymphatic vessels and observed predominantly in upper extremities. The infiltration and preferential M2 differentiation of macrophage are observed in chronic lymphedema, and lymphedema is considered a causative factor of intralymphatic histiocytosis. However, what causes accumulation of histiocytes in the lymphatic vessels remains unclear, and investigation regarding the characteristics of the macrophages has not been evaluated. We present a case of intralymphatic histiocytosis, in which immunohistochemical staining for both macrophages and lymphatic vessels was performed to evaluate the nature of macrophages within lymphatic vessels and to determine the causative factor. Aggregated macrophages were shown to be M2 macrophages positive for CD68, CD163 and CD206 but negative for inducible nitric oxide synthase. Thick lymphatic vessels positive for D2‐40 and α‐SMA in the superficial dermis were observed. We speculate that chronic lymphedema leads to hypertrophy of lymphatic vessels with smooth muscle in the superficial dermis, which may be a kind of malformation, and these lymphatic vessels produce some chemokines that induce intralymphatic aggregation of macrophages. 相似文献
96.
Patients with X‐linked hyperimmunoglobulin M syndrome (XHIGM) have a defective CD40–CD40 ligand system and further immunoglobulin class‐switching. They may present with recurrent infection and malignancy involving the liver, pancreas or biliary tract. We report here a case of poorly differentiated transitional cell carcinoma in a young man with XHIGM even on regular treatment and discuss the possible pathogenesis. Given that the triggering of the CD40–CD40 ligand system has been found to improve tumor immunogenicity in recent studies, future immunotherapy targeting the CD40 ligand for these patients may be feasible to prolong their survival. 相似文献
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Sanne Jespersen Bo Langhoff Hnge Candida Medina David da Silva T Faustino Gomes Correira Alex Lund Laursen Christian Erikstrup Lars
stergaard Christian Wejse 《Journal of the International AIDS Society》2015,18(1)
Introduction
With more people receiving antiretroviral treatment (ART), the need to detect treatment failure and switch to second-line ART has also increased. We assessed CD4 cell counts (as a marker of treatment failure), determined the rate of switching to second-line treatment and evaluated mortality related to treatment failure among HIV-infected patients in Guinea-Bissau.Methods
In this retrospective cohort study, adult patients infected with HIV-1 receiving ≥6 months of ART at an HIV clinic in Bissau were included from June 2005 to July 2014 and followed until January 2015. Treatment failure was defined as 1) a fall in CD4 count to baseline (or below) or 2) CD4 levels persistently below 100 cells/µL after ≥6 months of ART. Cox hazard models, with time since six months of ART as the time-varying coefficient, were used to estimate the hazard ratio for death and loss to follow-up.Results
We assessed 1,591 HIV-1-infected patients for immunological treatment failure. Treatment failure could not be determined in 594 patients (37.3%) because of missing CD4 cell counts. Among the remaining 997 patients, 393 (39.4%) experienced failure. Only 39 patients (9.9%) with failure were switched from first- to second-line ART. The overall switching rate was 3.1 per 100 person-years. Mortality rate was higher in patients with than without treatment failure, with adjusted hazard rate ratios (HRRs) 10.0 (95% CI: 0.9–107.8), 7.6 (95% CI: 1.6–35.5) and 3.1 (95% CI: 1.5–6.3) in the first, second and following years, respectively. During the first year of follow-up, patients experiencing treatment failure had a higher risk of being lost to follow-up than patients not experiencing treatment failure (adjusted HRR 4.4; 95% CI: 1.7–11.8).Conclusions
We found a high rate of treatment failure, an alarmingly high number of patients for whom treatment failure could not be assessed, and a low rate of switching to a second-line therapy. These factors could lead to an increased risk of resistance development and excess mortality. 相似文献100.
Reshma Naik Tanya Doherty Debra Jackson Hanani Tabana Sonja Swanevelder Donald M Thea Frank G Feeley Matthew P Fox 《Journal of the International AIDS Society》2015,18(1)