儿童特发性血小板减少性紫癜病因及治疗进展

小儿特发性血小板减少性紫癜（ITP）是儿童时期最常见的出血性疾病。大多数ITP患儿愈后较好而部分患儿则转为难治性ITP。该病的病因和发病机制可能与多种因素诱发机体体液免疫和细胞免疫紊乱有关。治疗方法主要有糖皮质激素、免疫抑制剂以及脾切除等。     

特发性血小板减少性紫癜细胞免疫异常与胸腺肽α1应用的研究进展

特发性血小板减少性紫癜（ITP）是一类由自身抗体导致的血小板在网状内皮系统被吞噬破坏的自身免疫性出血性疾病，迄今为止，发病机制尚未完全阐明。以往着重探讨体液免疫功能紊乱与ITP发病的密切关系，现在越来越多的资料表明除体液免疫机制外，在ITP细胞免疫起了非常重要的作用，ITP患者在T细胞亚群、细胞因子、NK细胞等多方面都可发现异常。     

特发性血小板减少性紫癜发病机制

特发性血小板减少性紫癜（ITP）是一种获得性的自身免疫性疾病,其特点为血小板数目减少和皮肤粘膜的出血。发病率约为1／10000。对于ITP的发病机制目前认为体液免疫仍然是ITP发病的主要原因,其中包括抗原呈递细胞、T细胞和B细胞之间的相互作用。近年来越来越多的证据表明,调节性T细胞起着非常重要的作用,T细胞介导的细胞毒性反应也被证实参与了ITP患者血小板的破坏过程。此外,抗原递呈细胞的功能紊乱、巨核细胞的异常和幽门螺杆菌感染也和ITP的发病有关。     

成人原发免疫性血小板减少症的治疗新进展

原发免疫性血小板减少症(ITP)是一种常见的出血性疾病,随着发病机制研究的深入,在原有治疗基础上又有了新的进展。本文从临床试验、专家共识角度对ITP的发病机制、治疗现状及展望综述如下。     

原发免疫性血小板减少症的治疗进展

原发免疫性血小板减少症(ITP)是一种常见的出血性疾病,随着发病机制研究的深入,ITP临床治疗在原有基础上近年又有了新的进展。本文综述ITP临床药物治疗进展。     

重组人血小板生成素治疗儿童免疫性血小板减少症临床观察

<正>免疫性血小板减少症(ITP)是一种常见的获得性免疫介导的出血性疾病,致死性并发症为颅内出血[1]。以往认为ITP的发病机制主要是抗体介导的血小板破坏增多;近年来研究发现ITP发病还存在血小板无效生成,研究表明ITP患者的血清可抑制巨核细胞生长,认为这与血小板自身抗体在致敏血小板的同时还可致敏骨髓巨核细胞,影响后者的增殖和分     

微小RNA在免疫性血小板减少症发病机制中的研究进展

摘要：免疫性血小板减少症（ITP）是由于血小板破坏增加或生成减少导致外周血血小板的减少，引起皮肤、黏膜 及内脏出血等临床表现为特点的常见出血性疾病。ITP的发病机制迄今为止尚未得到完全阐明，积极探索本病的发 病机制，不仅具有重要的理论意义，而且可能为本病的治疗提供新的策略。微小RNA（microRNA，miRNA）是一类长 度约为19~22个核苷酸的小分子非编码RNA，通过调控其靶基因，参与多种疾病的发生和发展。目前miRNA在ITP 发病机制中的研究越来越广泛，本文就近年来针对miRNA在ITP发病机制中的研究进展做一综述。     

肺动脉高压的免疫调节治疗

肺动脉高压是临床上常见的疾病,其发病机制尚未完全清楚。免疫因素在肺动脉高压的发病机制中起重要作用。免疫抑制疗法为肺动脉高压治疗提供了新的途径。本文就机体免疫紊乱对肺动脉高压的影响机制及其免疫调节治疗的临床应用及研究现状进行综述。     

慢性难治性原发性免疫性血小板减少症治疗进展

原发性免疫性血小板减少症(Primary immune thrombocytopenia,ITP)原称特发性血小板减少性紫癜(Idiopathic thrombocytopenic purpura,ITP),是一种自身免疫性疾病,是由于机体免疫系统功能紊乱引起血小板破坏增多致其数目减少引起的出血性疾病,临床表现为皮肤黏膜瘀点、瘀斑,尿血,严重者可引起内脏和颅内出血危及生命,骨髓象表现为巨核细胞发育、成熟障碍。儿童急性ITP大多预后良好,75%~82%急性ITP 6个月内可获得缓解,持续6个月以上的ITP中超过1/4在     

干扰素α-2b对复发性阿弗他溃疡患者外周血T细胞亚群的影响

<正>复发性阿弗他溃疡(RAU)是一种常见的口腔黏膜疾病,患病率居口腔黏膜疾病之首,有癌变可能,其病因与致病机制尚未完全明确[1]。目前认为其发病与病毒感染、焦虑、疲劳、内分泌紊乱及机体免疫功能障碍等因素有关,其中免疫学发病机制,尤其T细胞亚群的调节紊乱已引起广泛关注[2]。     

血小板相关抗体、巨核细胞数量对免疫性与非免疫性血小板减少患者的诊断意义

目的比较骨髓巨核细胞数量、血小板相关抗体在免疫性血小板减少和非免疫性血小板减少患者中的不同,探讨巨核细胞数量、血小板相关抗体在血小板减少症诊断中的意义。方法观察132例ITP患者及48例非ITP患者的骨髓巨核细胞数量、血小板相关抗体水平,进行统计分析。结果 132例ITP患者中巨核细胞数量正常者35例,增多者78例,77例ITP患者中血小板抗体阳性58例。结论由于血小板抗体生成使ITP患者巨核细胞成熟障碍,因此血小板生成减少,骨髓巨核细胞数量在免疫性血小板减少的诊断中是必要的检查,血小板抗体与巨核细胞数量相关。     

免疫性血小板减少性紫癜合并幽门螺旋杆菌感染患儿免疫功能及研究

目的分析免疫性血小板减少性紫癜合并幽门螺旋杆菌感染的患儿淋巴细胞免疫功能的变化。方法健康体检组为对照组。免疫性血小板减少性紫癜组为观察组及合并HP感染的ITP组为治疗组。在常规激素治疗基础上给予三联抗HP治疗。流式细胞仪检测患儿合并HP感染的CD4+,CD19+等抗体表达。结果 ITP组及合并HP感染的ITP组CD4+下降,CD4+/CD8+下降,CD19+升高与对照组相比有统计学意义,观察组与治疗组比较,HP感染的ITP组在CD4+/CD8+比值下降及CD19+增高较之ITP组更为明显,两组比较有统计学意义。结论 ITP患儿合并HP感染大多存在细胞及体液免疫功能异常。     

急性免疫性血小板减少症患儿NK细胞、NK样T细胞数量变化及槐杞黄联合糖皮质激素疗效探讨

目的探讨NK样T细胞及NK细胞数量变化对儿童急性免疫性血小板症(ITP)发病的影响,观察槐杞黄口服联合糖皮质激素对儿童ITP疗效的影响。方法采用前瞻性对照研究的方法,收集2016年1-12月于我科确诊并住院治疗的70例ITP患儿及门诊健康体检的30例正常儿童资料,均在未接受任何治疗时采集外周血,检测淋巴细胞亚群、NK样T细胞数值并进行分析比较。将70例ITP患儿随机分成观察组和对照组,每组35例。实验组在常规的糖皮质激素治疗方法基础上加用槐杞黄口服,对照组则仅为激素方法治疗。治疗期间观察两组患儿临床情况,定期于清晨空腹采血,记录血小板计数,同时采用流式细胞仪技术,检测淋巴细胞亚群、NK样T细胞的表达率。结果 ITP儿童外周血中NK细胞(6.2%±1.37%)、NK样T细胞的数量(0.98%±0.41%)较健康儿童(15.92%±3.84%,3.56%±0.78%)明显下降,总B细胞数量则明显上升,差异有统计学意义(P<0.05);观察组的有效率为94.3%,显著高于对照组的85.7%,平均住院治疗时间缩短;治疗后,ITP患儿外周血NK细胞、NK样T细胞的表达率均显著升高(P<0.05);治疗期间观察组血小板计数恢复正常范围及NK细胞和NK样T细胞数量上升较对照组明显,差异有统计学意义(P<0.05)。结论 NK细胞及NK样T细胞数量下降可能与儿童ITP发病相关,槐杞黄联合糖皮质激素治疗儿童ITP,可能通过改善免疫功能紊乱,提升NK细胞、NK样T细胞数量,加快血小板计数的恢复,进而缩短疗程。     

Role of Nucleotide-binding and Oligomerization Domain 2 Protein (NOD2) in the Development of Atherosclerosis

NOD2 (nucleotide-binding and oligomerization domain 2) was initially reported as a susceptibility gene for Crohn''s disease, with several studies focused on elucidating its molecular mechanism in the progression of Crohn''s disease. We now know that NOD2 is an intracellular bacterial sensing receptor, and that MDP-mediated NOD2 activation drives inflammatory signaling. Various mutations in NOD2 have been reported, with NOD2 loss of function being associated with the development of Crohn''s disease and other autoimmune diseases. These results suggest that NOD2 not only has an immune stimulatory function, but also an immune regulatory function. Atherosclerosis is a chronic inflammatory disease of the arterial wall; its pathologic progression is highly dependent on the immune balance. This immune balance is regulated by infiltrating monocytes and macrophages, both of which express NOD2. These findings indicate a potential role of NOD2 in atherosclerosis. The purpose of this review is to outline the known roles of NOD2 signaling in the pathogenesis of atherosclerosis.     

The role of the neuroendocrine and immune systems in the pathogenesis of depression

Development of depression is associated with the body's response to prolonged stress, which adversely affects the functioning of the nervous, endocrine and immune systems. Prolonged stress can lead to the development of a so-called allostatic load and reduction of concentration of brain-derived neurotrophic factor. These changes result in impairment of neurogenesis and synaptic remodeling process. This article illustrates the involvement of key mediators of allostasis such as the neuroendocrine and immune systems, in the pathogenesis of depression. The literature concerning the contribution of the neuroendocrine and immune systems to depression incidence was reviewed. Development of depression is associated with disturbance of the body's allostasis and inflammatory activation of the immune system. It leads to a chronic increase in the concentration of cortisol and proinflammatory cytokines, which results in an allostatic load. This load leads to neurodegeneration, eventually causing irreversible cognitive impairment and permanent disability. Determination of the concentration of chemokines and their receptors is an important indicator of activation of the immune and neuroendocrine systems. The activity of these systems reflects the severity of the disease and provides important information for effective antidepressant treatment.     

LncRNA GAS5 inhibits Th17 differentiation and alleviates immune thrombocytopenia via promoting the ubiquitination of STAT3

BackgroundThe increased differentiation of T helper 17 cells (Th17) accelerates the development of immune thrombocytopenia (ITP), which is a common autoimmune disease with limited therapeutic methods. Recent studies have revealed that long non-coding RNAs (lncRNAs) play a critical role in autoimmune diseases, thus this study aims to investigate the effect of lncRNA GAS5 on the differentiation of Th17 cells in ITP.MethodsThe expression of GAS5 in peripheral blood mononuclear cells (PBMCs) of ITP patients and spleen tissues of ITP mice was measured by qRT-PCR. The percentage of Th17 cells in CD4⁺ cells was measured by flow cytometry. The combination between GAS5 and STAT3 was confirmed by RNA pull-down assay and RNA Binding Protein Immunoprecipitation (RIP). The ubiquitination of STAT3 was detected by ubiquitination assay and the interaction between STAT3 and TRAF6 was measured by Co-Immunoprecipitation (Co-IP). Finally, the effect of GAS5 on Th17 differentiation was investigated in vitro and in vivo using lentivirus (lenti)-GAS5.ResultsGAS5 expression was downregulated both in PBMCs of ITP patients and spleen tissues of ITP mice. Overexpression of GAS5 suppressed Th17 differentiation while had no effect on Treg differentiation in naïve CD4⁺ cells. RNA pull-down and RNA immunoprecipitation assays confirmed the interaction between GAS5 and STAT3. Further studies showed GAS5 accelerated the degradation of STAT3 via promoting TRAF6-mediated ubiquitination. Overexpressing GAS5 suppressed Th17 differentiation in vitro and alleviated ITP in vivo via reducing STAT3.ConclusionLncRNA GAS5 inhibited Th17 differentiation through promoting the TRAF6-mediated ubiquitination of STAT3, thus relieving ITP.     

Pharmacokinetic and pharmacodynamic effects of high-dose monoclonal antibody therapy in a rat model of immune thrombocytopenia

Intravenous administration of pooled, polyvalent human immunoglobulin (IVIG) has been used for over 20 years as a therapy for immune thrombocytopenia (ITP). IVIG is available in limited quantities, and clinical preparations have been associated with the transfer of human pathogens. We have proposed that high-dose monoclonal antibody may be used in lieu of IVIG to achieve beneficial effects in the treatment of ITP. The current study investigates the effects of high-dose monoclonal antibody therapy in a rat model of ITP. Hybridoma cells secreting a murine monoclonal antiplatelet antibody (7E3) and murine monoclonal anti-methotrexate IgG (AMI) were grown in serum-free media. Next, 7E3, 8 mg kg(-1), was administered intravenously to rats following pretreatment with saline or AMI (1 g kg(-1) IV). AMI and 7E3 plasma concentrations were determined via enzyme-linked immunosorbent assay, and platelet count was determined with a Cell-Dyne hematology analyzer. Severe, transient thrombocytopenia was induced by 7E3. Platelet counts dropped to approximately 8% of initial values within 1 hour after 7E3 administration. AMI pretreatment dramatically affected 7E3-induced thrombocytopenia, significantly altering the time course of thrombocytopenia (P < .05) and significantly decreasing the severity of 7E3-induced thrombocytopenia (ie, following AMI pretreatment, nadir platelet count was greater than 8-fold that of the control group, P < .05). In addition, AMI pretreatment induced a 57% increase in 7E3 clearance (1.13 +/- 0.13 mL h(-1) kg(-1) vs 0.72 +/- 0.08 mL h(-1) kg(-1), P < .05). Consequently, high-dose monoclonal antibody therapy attenuated thrombocytopenia and produced a moderate increase in the clearance of antiplatelet antibodies in a rat model of ITP.     

复发性流产的免疫机制和药物治疗进展

复发性流产(Recurrent spontaneous abortion,RSA)是指妊娠140 d之前两次及以上的自然流产,发病几率逐年升高,其发病原因复杂,包括子宫畸形、激素和代谢紊乱、感染因素、抗磷脂综合症以及细胞遗传学变异等,但是40%~60%的复发性流产的发病机制尚不明确,对其免疫机制的研究是近年来的研究重点。生殖免疫学认为妊娠是一种半同种移植过程,母-胎界面的免疫耐受可以维持妊娠的继续,打破这种免疫耐受会导致复发性流产的发生。复发性流产的免疫发生机制主要与抗磷脂抗体、自然杀伤细胞、调节性T细胞、滤泡辅助性T细胞以及细胞因子有关,对其进行免疫调节治疗可以降低流产率。文章对RSA的免疫机制的研究和药物治疗提供系统性的总结,包括抗凝血药物、免疫疗法、激素疗法和干细胞疗法等。