淋巴细胞功能测定对小儿过敏性紫癜诊断与治疗的价值初探

目的研究过敏性紫癜(HSP)患儿急性期外周血淋巴细胞功能的变化,探讨其在HSP诊断与治疗中的意义。方法采用流式细胞术(FCM)对51例HSP患儿急性期和40例健康查体儿童外周血淋巴细胞亚群CD3+、CD4+、CD8+、CD4+/CD8+、CD19+和NK细胞(CD16++CD56+)进行检测。结果与对照组儿童比较,HSP患儿急性期外周血CD4+、CD4+/CD8+及NK细胞(CD16++CD56+)数量明显减低(P0.01),CD8+和CD19+细胞比率明显增高(P0.05,P0.01)。结论 HSP患儿急性期存在免疫功能紊乱,外周血淋巴细胞功能测定对HSP患儿的早期诊断与治疗有重要意义。     

骨髓增生异常综合征NK细胞及亚群检测意义分析

目的 分析骨髓增生异常综合征患者外周血NK/Lym%及CD56dim+CD16+NK/CD56bri+CD16-NK检测的意义。方法 研究对象为74例骨髓增生异常综合征（Myelodysplastic syndrome,MDS）患者,选取50例健康人为对照组。应用流式细胞术检测CD3+T、CD19+B、CD56dim+CD16+NK、CD56bri+CD16-NK数量并计算NK/Lym%及CD56dim+CD16+NK/CD56bri+CD16-NK比值。分析其在MDS和对照组之间的差异、MDS患者治疗前后的差异以及IPSS-R极低危/低危组,中危组,高危/极高危组之间的差异。结果 MDS组NK/Lym%和CD56dim+CD16+NK/CD56bri+CD16-NK亚群比例低于对照组,经过治疗后达到OR组,比例升高,在IPSS-R各种中随着危险度升高,比例减低,但无统计学意义。结论 外周血NK细胞比例及功能的改变与MDS的发病相关,且是疾病治疗效果监测的重要实验室指标。     

IL-12及NK细胞检测在手足口病诊治中的价值

目的:检测手足口病患儿外周血细胞因子IL-12及NK细胞水平,探讨其免疫功能变化及临床意义。方法:根据病情将手足口病患儿分为轻症组、重症组,以健康儿童作为对照;采用流式细胞术检测患儿外周血CD16+CD56+细胞的相对计数;采用ELISA方法检测血清中IL-12水平。结果:重症组患儿血清中IL-12水平显著高于轻症组和对照组(P<0.01,P<0.05),重症组患儿IL-12水平治疗后显著降低(P<0.05);重症组患儿外周血CD16+CD56+细胞的相对计数虽然低于轻症组和对照组,但差异无统计学意义(P﹥0.05),而经治疗后显著降低(P<0.05)。结论:手足口病患儿外周血IL-12和NK细胞水平随患儿的免疫功能紊乱而发生变化,观察外周血IL-12和NK细胞的变化在手足口病的诊断、治疗和病情转归方面具有一定的参考价值。     

应用流式细胞术辅助诊断神经母细胞瘤患儿骨髓侵犯

目的应用CD45/CD56/CD81/GD2四色组合方案的流式细胞术诊断神经母细胞瘤(NB)患儿骨髓侵犯,并评估其准确性。方法连续纳入2019年6月至2020年6月首都医科大学附属北京儿童医院肿瘤内科收治且确诊为NB患儿120例,诊断初期行骨髓细胞形态学(包括骨髓涂片和骨髓活检免疫组化)检测。应用CD45/CD56/CD81/GD2四色组合方案的流式细胞术对采集的NB患儿骨髓标本进行检测分析,并与细胞形态学结果进行比较。采用SPSS 13.0统计学软件进行数据处理,一致性分析采用Kappa检验。结果在37例骨髓细胞形态学阳性NB患儿组中,流式细胞术结果阳性34例,准确率为91.8%;83例骨髓细胞形态学阴性患儿组中,流式细胞术结果阴性82例,准确率为98.7%。流式细胞术与骨髓细胞形态学结果具有较强的一致性(Kappa=0.921,P0.001)。结论应用CD45/CD56/CD81/GD2四色组合方案的流式细胞术能够快速、准确诊断NB患儿骨髓侵犯,并可弥补骨髓细胞学检查的不足。     

类风湿性关节炎患者外周血CD3~+ CD(16、56)~+ NK T细胞百分率的变化及意义

目的探讨CD3+CD(16、56)+自然杀伤(NK)T细胞在类风湿性关节炎(RA)患者外周血中的变化及意义。方法采用流式细胞术检测RA患者(病情活动组和病情稳定组)及健康人(对照组)外周血淋巴细胞中CD3+CD(16、56)+细胞的比例及CD3+CD(16、56)+淋巴细胞CD69的表达百分率。结果 RA病情活动组外周血CD3+CD(16、56)+NK T细胞的比例及NK T细胞CD69的表达百分率明显低于RA病情稳定组及健康对照组(P均<0.01);RA病情稳定组NK T细胞的比例及NK T细胞CD69的表达百分率与健康对照组差异无统计学意义(P均>0.05)。结论 RA患者外周血中CD3+CD(16、56)+NK T细胞比例减少及活性受抑制可能参与了RA的发病过程,且可能与RA的病情活动性相关。     

CD16CD56NK细胞在重症肌无力发病机制中的作用

目的:研究重症肌无力(MG)患者外周血CD16+CD56+ NK细胞的水平,及其在MG发病机制中的作用.方法:应用流式细胞仪检测16例MG患者与20名正常对照外周血CD16+CD56+NK细胞的百分率.结果:MG组外周血CD16+CD56+NK细胞百分率(13.81±5.59)%明显高于对照组的(7.23±1.95)%,P <0.05.结论:NK细胞在MG发病中起重要作用,既可通过分泌IFN2γ等细胞因子途径促进MG的发病,也可通过细胞毒作用发挥免疫效应.     

淋巴细胞亚群联合检测对脓毒症患者不良预后的评估价值

目的 探讨T、B和NK淋巴细胞亚群相关指标对脓毒症患者不良预后的预测价值.方法 应用前瞻性研究方法,选取宁夏人民医院急诊重症监护室(EICU)及ICU共101例脓毒症患者为对象,检测入院48 h内外周血T、B和NK淋巴细胞亚群相关指标水平,随访至出院,观察指标异常对死亡结局的危险度,评估各指标联合检测对死亡风险的预测价值.结果 脓毒性休克患者CD3、CD3 +/CD4+低于脓毒症组和严重脓毒症组,严重脓毒症和脓毒性休克患者CD3 +/CD8+,CD3-/CD19+,CD4 +/CD8+低于脓毒症组,CD (16+56)+高于脓毒症组(P＜0.05);死亡患者的单核细胞高于生存患者,CD3、CD3-/CD19+、CD3 +/CD4+、CD4 +/CD8+低于生存患者(P＜0.05); CD3-/CD19+、CD3 +/CD8、CD4 +/CD8+为脓毒症预后的保护因素,OR值分别0.235、0.006、0.108;淋巴细胞亚群联合预测因子、APACHEⅡ评分、SOFA评分对死亡风险预测效能的ROC曲线下面积分别为0.993、0.877、0.848;淋巴细胞亚群联合判别函数对病情程度的误判率为19.8％,对患者结局的误判率为4％.结论 脓毒症患者淋巴细胞亚群表达异常,淋巴细胞亚群的联合检测对脓毒症患者的病情及预后有指导价值.     

全身型幼年特发性关节炎临床及治疗特点

目的 探讨全身型幼年特发性关节炎（SOJIA）临床与治疗特点.方法 回顾性分析65例SOJIA患儿的临床表现、实验室检查及治疗方法与随访结果.结果 仅22例（33.8％）临床同时出现典型三联征,43例（66.2％）患儿临床表现不典型,其中12例（18.5％）患儿因临床表现不典型而贻误诊断.采用个体化治疗方案：非甾体类抗炎药（NSAIDs）＋糖皮质激素7例（10.8％）；NSAIDs＋甲氨蝶呤（MTX） 15例（23.1％）；NSAIDs＋MTX＋糖皮质激素43例（66.2％）,其中8例应用大剂量甲泼尼龙冲击治疗,8例因病情反复而加用环孢素A治疗.23例（35.4％）联合应用丙种球蛋白治疗.64例（98.5％）患儿初治均获缓解.53例随访4个月～7年,29例（54.7％）持续缓解,24例（45.3％）复发.结论 SOJIA非典型病例早期诊断存在困难,NSAIDs＋抗风湿药物＋糖皮质激素联合用药是目前较为推崇的治疗方案,但远期疗效差,复发率较高,生物制剂有望改善预后.     

手足口病患儿血清细胞因子及自然杀伤细胞表达的变化及临床意义

目的观察手足口病(HFMD)患儿血清细胞因子及自然杀伤(NK)细胞表达的变化,并探讨其临床意义。方法将56例HFMD患儿根据病情轻重分为轻症组31例和重症组25例,另选取同期健康体检儿童30例设为对照组,分别检测3组血清白细胞介素(IL)-6、IL-12、肿瘤坏死因子-α(TNF-α)水平及CD16+CD56+含量,并分析各指标与病情的相关性。结果轻症组血清IL-6、IL-12、TNF-α水平显著高于重症组及对照组,重症组仅IL-12水平高于对照组;重症组CD16+CD56+细胞含量显著高于轻症组和对照组,差异均有统计学意义(P0.01)。相关性分析结果表明,IL-6和TNF-α表达水平与病情严重程度呈负相关(r=-0.467,-0.518,P0.01)。结论 HFMD患儿血清细胞因子表达水平及免疫功能紊乱,检测IL-6、IL-12、TNF-α水平及CD16+CD56+含量有助于识别重症HFMD。     

手足口病患儿细胞免疫功能的改变及其临床意义

目的 探讨手足口病(HFMD)患儿细胞免疫功能状况.方法 选取HFMD患儿186例为观察组,同期体检儿童140名为健康对照组,观察组分为重症病例组和普通病例组及EV7阳性组和EV71阴性组,采用流式细胞术分别检测各组患儿T(CD3+)淋巴细胞、Th(CD4+)细胞、Ts(CD8+)细胞、NK(CD16+)细胞数量及其所占淋巴细胞的百分比;计算CD4+/CD8+比值.结果 观察组的CD3+、CD4+、CD16+低于健康对照组(P＜0.05),重症病例组CD3+、CD4+、CD16+低于普通病例组(P＜0.05或P＜0.01).EV71阳性组的CD3+、CD4+、CD16+低于EV71阴性组差异有统计学意义(P＜0.05或P＜0.01).结论 HFMD患儿细胞免疫功能降低,重症组和EV71阳性组尤其明显,细胞免疫功能状况可作为判断病情和预后的重要指标.     

Obesity = physical activity + dietary intake + sleep stages + light exposure

Daily levels of physical activity and calories from dietary intake have been the focus of obesity prevention measures. Recent findings have made a twist in the line of thinking. The timing of physical exercise and that of dietary intake are also important to obesity prevention. Night-time sleep and exposure to light are therefore important targets of intervention.     

In vivo equilibrium of proinflammatory IL-17+ and regulatory IL-10+ Foxp3+ RORgamma t+ T cells

The nuclear hormone receptor retinoic acid receptor-related orphan receptor gamma t (RORgamma t) is required for the generation of T helper 17 cells expressing the proinflammatory cytokine interleukin (IL)-17. In vivo, however, less than half of RORgamma t(+) T cells express IL-17. We report here that RORgamma t(+) T alphabeta cells include Foxp3(+) cells that coexist with IL-17-producing RORgamma t(+) T alphabeta cells in all tissues examined. The Foxp3(+) RORgamma t(+) T alphabeta express IL-10 and CCL20, and function as regulatory T cells. Furthermore, the ratio of Foxp3(+) to IL-17-producing RORgamma t(+) T alphabeta cells remains remarkably constant in mice enduring infection and inflammation. This equilibrium is tuned in favor of IL-10 production by Foxp3 and CCL20, and in favor of IL-17 production by IL-6 and IL-23. In the lung and skin, the largest population of RORgamma t(+) T cells express the gammadelta T cell receptor and produce the highest levels of IL-17 independently of IL-6. Thus, potentially antagonistic proinflammatory IL-17-producing and regulatory Foxp3(+) RORgamma t(+) T cells coexist and are tightly controlled, suggesting that a perturbed equilibrium in RORgamma t(+) T cells might lead to decreased immunoreactivity or, in contrast, to pathological inflammation.     

Rh33 in two of three German siblings with D+ C+ c+ E− e+ red cells

The proposita in a German family of three siblings has D+ C+ c+ E- e+ f+ Rh: -17,19,33,34 red cells with weak C, e, f, Rh19, and Rh34 and stronger-than-usual Rh33 expression. One sibling has D+ C+ c+ E- e+ f+ Rh:17,19,33,34 red cells with weak f and ordinary-strength Rh33, and the other sibling has D+ C+ c+ E- e+ f+ Rh:17,19,-33,34 red cells. In the absence of any further family members, the proposita's unusual phenotype suggests that she has an RoHar haplotype and a "new" Rh haplotype, provisionally named R1Lisa, that encodes Rh33, normal-strength D, weak C, weak or nondemonstrable e, Rh19, and Rh34, but not Rh17. Her Rh:33 sibling may have R1 and RoHar and her Rh:-33 sibling R1 and r haplotypes.     

CD4+CD25+和CD8+调节性T细胞的作用机制

调节性T细胞（Treg）主要在机体免疫系统中发挥负向调节作用,既能抑制不恰当的免疫反应,又能限定免疫应答的范围、程度及作用时间,对CD4^＋和CD8^＋效应性T淋巴细胞的增殖起抑制作用,因此在移植物抗宿主病、自身免疫病、过敏性疾病等的发病机制和临床治疗中有潜在的应用价值.本文重点介绍CD4^＋CD25^＋Treg和CD8^＋Treg的作用机制,并简述调节性T细胞研究面临的挑战与展望.     

Normal human dermis contains distinct populations of CD11c+BDCA-1+ dendritic cells and CD163+FXIIIA+ macrophages

We used a panel of monoclonal antibodies to characterize DCs in the dermis of normal human skin. Staining for the CD11c integrin, which is abundant on many kinds of DCs, revealed cells in the upper dermis. These cells were positive for blood DC antigen-1 (BDCA-1; also known as CD1c), HLA-DR, and CD45, markers that are also expressed by circulating myeloid DCs. A small subset of CD11c+ dermal cells expressed DEC-205/CD205 and DC-lysosomal-associated membrane glycoprotein/CD208 (DC-LAMP/CD208), suggesting some differentiation or maturation. When BDCA-1+ cells were selected from collagenase digests of normal dermis, they proved to be strong stimulators for T cells in a mixed leukocyte reaction. A second major population of cells located throughout the dermis was positive for factor XIIIA (FXIIIA), but lacked CD11c and BDCA-1. They expressed the macrophage scavenger receptor CD163 and stained weakly for HLA-DR and CD45. Isolated CD163+ dermal cells were inactive in stimulating T cell proliferation, but in biopsies of tattoos, these cells were selectively laden with granular pigments. Plasmacytoid DCs were also present in the dermis, marked by CD123 and BDCA-2. In summary, the normal dermis contains typical immunostimulatory myeloid DCs identified by CD11c and BDCA-1, as well as an additional population of poorly stimulatory macrophages marked by CD163 and FXIIIA.     

Allograft rejection is restrained by short-lived TIM-3+PD-1+Foxp3+ Tregs

Tregs play a pivotal role in inducing and maintaining donor-specific transplant tolerance. The T cell immunoglobulin and mucin domain-3 protein (TIM-3) is expressed on many fully activated effector T cells. Along with program death 1 (PD-1), TIM-3 is used as a marker for exhausted effector T cells, and interaction with its ligand, galectin-9, leads to selective death of TIM-3+ cells. We report herein the presence of a galectin-9-sensitive CD4+FoxP3+TIM-3+ population of T cells, which arose from CD4+FoxP3+TIM-3- proliferating T cells in vitro and in vivo and were often PD-1+. These cells became very prominent among graft-infiltrating Tregs during allograft response. The frequency and number of TIM-3+ Tregs peaked at the time of graft rejection and declined thereafter. Moreover, these cells also arise in a tolerance-promoting donor-specific transfusion model, representing a pool of proliferating, donor-specific Tregs. Compared with TIM-3- Tregs, TIM-3+ Tregs, which are often PD-1+ as well, exhibited higher in vitro effector function and more robust expression of CD25, CD39, CD73, CTLA-4, IL-10, and TGF-β but not galectin-9. However, these TIM-3+ Tregs did not flourish when passively transferred to newly transplanted hosts. These data suggest that a heretofore unrecognized graft-infiltrating, short-lived subset of Tregs can restrain rejection.