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关键词： 重症肺炎支原体肺炎   25-羟维生素D_(3)   白细胞介素-21   预后  

摘要： 目的 分析重症肺炎支原体肺炎(MPP)患儿血清25-羟维生素D_(3)[25 (OH) D_(3)]、白细胞介素-21(IL-21)水平与预后的相关性。方法 选取2023年1月至2024年1月安徽医科大学第一附属医院儿科收治的111例重症MPP患儿(病例组)和107例轻症MPP患儿(对照组)为研究对象,随访3个月后根据预后情况将病例组患儿分为预后不良亚组(n=26)和预后良好亚组(n=85)。比较病例组和对照组患儿入院时血清25 (OH) D_(3)和IL-21水平、小儿危重症评分(PCIS)、肺炎严重指数(PSI)评分,并分析血清25 (OH) D_(3)、IL-21水平与PCIS、PSI评分的相关性;比较预后不良亚组和预后良好亚组入院时一般资料、血清炎性因子[C-反应蛋白(CRP)、白细胞介素-6(IL-6)]、25 (OH) D_(3)、IL-21水平,采用Logistic回归模型分析病例组患儿预后不良的影响因素;绘制受试者工作特征曲线(ROC)分析病例组患儿入院时血清25 (OH) D_(3)、IL-21、CRP、IL-6预测预后不良的价值。结果 病例组血清25 (OH) D_(3)水平、PCIS评分均低于对照组,血清IL-21水平、PSI评分均高于对照组(P<0.05);病例组和对照组血清25 (OH) D_(3)水平与PCIS评分呈正相关,与PSI评分呈负相关(P<0.05);血清IL-21水平与PCIS评分呈负相关,与PSI评分呈正相关(P<0.05);病例组患病后3个月预后不良率为23.42%;预后不良亚组血清25 (OH) D_(3)水平和PCIS评分均低于预后良好亚组(P<0.05),血清IL-21、CRP、IL-6水平和PSI评分均高于预后良好亚组(P<0.05);多因素Logistic回归分析显示,血清25 (OH) D_(3)、IL-21、CRP、IL-6水平均为重症MPP患儿预后不良的影响因素(P<0.05);ROC曲线分析显示,病例组血清25 (OH) D_(3)联合IL-21预测预后不良的曲线下面积(AUC)为0.876,均高于25 (OH) D_(3)、IL-21、CRP、IL-6单独预测的AUC(P<0.05)。结论 血清25 (OH) D_(3)和IL-21水平与重症MPP患儿病情严重程度及预后密切相关,联合检测可提高预后不良的预测效能。

关键词： 慢性炎症   细胞因子   慢性疾病   抗炎饮食  

摘要： 研究发现,饮食在慢性炎症的发展中起到了重要作用,因此,通过改变饮食来减少炎症是可行的。“抗炎饮食”中的“炎”和平时嗓子发炎的“炎”不同,是指各种细胞因子在压力或应激状态下过量产生的低水平慢性炎症。研究发现,这种反复持续的慢性炎症与多种慢性疾病有关,如心血管疾病、癌症等。

关键词： 关键技术培训班   大兴生物医药基地  

摘要： 7月12日,为助力业内企业快速对接国际前沿技术标准,中国医药生物技术协会、中关村科技园区大兴生物医药产业基地管理委员会联合主办了《肿瘤浸润淋巴细胞(TIL)制剂制备和质量控制指南》发布暨肿瘤浸润淋巴细胞关键技术培训班。中国医药生物技术协会秘书长赵北海,大兴生物医药基地公司副总经理李海涛,北京佑安医院副院长张永宏,北京大学医学部免疫学系教授王月丹,四川大学遗传学教授、欧洲科学院院士丁显平,中国人民解放军联勤保障部队北戴河康复疗养中心大校徐扬,北戴河医院院长宋长兴,解放军总医院和哈尔滨医科大学附属肿瘤医院等国内知名专家,北京循生医学研究院院长张秀军,上海君赛生物科技有限公司总监何周出席会议。原卫生部副部长曹泽毅发来视频致辞。

关键词： 哮喘   气道上皮细胞   细胞因子  

摘要： 哮喘是一种常见的慢性气道炎症性疾病,其主要特点是气道的非特异性炎症、气道结构重塑及气道高反应性。多年来关于哮喘的发病机制主要集中于过敏反应导致的免疫失衡,而近年来针对气道上皮损伤在哮喘发生发展中的作用及机制受到重视,认为它可能是哮喘发病与控制的关键因素。气道上皮是人体呼吸系统抵御外界环境有害刺激的第一道屏障,也是气道最为重要的结构细胞。当哮喘患者吸入外界有害物质及过敏原时,气道上皮细胞首先受到侵犯并出现损伤,合成和释放多种炎性介质和细胞因子激活免疫细胞,诱导哮喘发生发展。本文旨在对目前有关哮喘气道上皮损伤的发生机制以及哮喘患者气道上皮的病理变化及其关键细胞因子进行综述,以发现潜在的生物标记物与治疗靶点,为哮喘的早期预测和精准防治提供依据。

关键词： 脓毒症   中性粒细胞胞外诱捕网   C反应蛋白   T淋巴细胞   评估价值  

摘要： 目的探讨血清中性粒细胞胞外诱捕网(NETs)、C反应蛋白(CRP)、外周血CD4^(+)与脓毒症患儿病情严重程度及预后的评估价值。方法回顾性选取我院收治的124例脓毒症患儿作为研究对象,根据疾病严重程度分为脓毒症组(n=49)、严重脓毒症组(n=30)、脓毒症休克组(n=45),比较三组一般资料及NETs、CRP、CD4^(+)水平,Spearman分析其与脓毒症患儿疾病严重程度的相关性。根据治疗28 d后生存情况分为生存组(n=74)和死亡组(n=50),比较两组一般资料及NETs、CRP、CD4^(+)水平,COX回归分析影响脓毒症患儿预后相关因素;ROC分析NETs、CRP、CD4^(+)联合检测对脓毒症患儿预后的预测价值;并绘制生存曲线分析不同血清NETs、CRP、外周血CD4^(+)水平脓毒症患儿预后情况。结果严重脓毒组血清NETs、CRP水平高于脓毒症组而低于脓毒症休克组,外周血CD4^(+)水平低于脓毒症组、高于脓毒症休克组(P<0.05);血清NETs、CRP水平与脓毒症疾病严重程度呈正相关,CD4^(+)水平呈负相关(r=0.280、0.468、-0.407,P<0.05);死亡组血清NETs、CRP水平比生存组更高,外周血CD4^(+)水平比生存组更低(P<0.05);血清NETs、CRP均是影响脓毒症患儿病情预后的相关因素(P<0.05);三者联合预测脓毒症病情预后的曲线下面积(AUC)值高于单项检测(P<0.05);血清NETs≤49.319%、CRP≤62.500 mg/L、外周血CD4^(+)≥24.481%者生存时间比血清NETs>49.319%、CRP>62.500 mg/L、外周血CD4^(+)<24.481%者更长(Z=25.795、29.135、15.883,P<0.05)。结论血清NETs、CRP、CD4^(+)与脓毒症患儿疾病严重程度有关,三者联合检测对脓毒症患儿病情及预后评估价值较高。

关键词： FAT10   UBD   proteasome   MHC-I   antigen processing   antigen presentation   cytotoxic T cells  

摘要： Introduction The presentation of pathogen-derived antigens on major histocompatibility complex (MHC) class I is crucial for the antiviral immune response. Degradation of intracellular pathogen-derived proteins by the 26S proteasome generates peptides that can be loaded on MHC-I molecules and presented to cytotoxic T cells. The cytokine-inducible ubiquitin-like modifier (ULM) HLA-F adjacent transcript 10 (FAT10) is encoded in the MHC locus and targets its substrates for proteasomal degradation. Therefore, it acts as an alternative signal for protein degradation, indicating a role in generating the peptide pool for MHC-I presentation. In this study, we aimed to elucidate the role of FAT10 in MHC class I *** Using different human and mouse cell lines deficient for FAT10, the effect of FAT10 on MHC-I surface expression and recovery was studied. For the evaluation of antigen presentation of viral and endogenous epitopes, T cell hybridoma assays and flow cytometry analysis were *** In our study, using model antigens and FAT10-deficient cells, we found that the absence of FAT10 does not affect the abundance of MHC-I molecules or the generation of endogenous and virus-derived MHC-I epitopes. Furthermore, we demonstrated that the cytotoxic T cell response to different viruses remains unchanged in FAT10-deficient mice compared to wild-type *** In summary, our findings indicate that the lack of FAT10 does not impact antigen presentation or the cytotoxic T-cell response across a number of different MHC-I-restricted peptides. Hence, we conclude that the contribution of FAT10 to MHC-I antigen presentation has previously been overestimated.

摘要： Objectives Blocking interleukin (IL)-6-receptor with tocilizumab has been a major advance in the treatment of giant-cell arteritis (GCA), supporting a crucial role of IL-6 receptor signalling. However, nearly half of the patients are not able to maintain glucocorticoid- free remission with tocilizumab. The impact of tocilizumab on vascular lesions of GCA is largely unknown since conflicting results have been obtained by imaging. The expression and functional role of IL-6-receptor in GCA immunopathology has not been previously investigated. This study aimed to investigate expression of IL-6 receptor in GCA and control arteries and to assess the impact of tocilizumab on ex vivo –cultured temporal arteries and aortic tissue from patients with GCA. Methods This study used a hypothesis-driven, candidate molecule transcriptomic approach using ex vivo temporal artery and aortic tissue culture, quantitative real-time polymerase chain reaction, immunofluorescence, Western Blot, immunoassay, adhesion, and chemotaxis assays. Results IL-6 receptor protein expressed intensively in GCA compared with that in control arteries. Tocilizumab decreased expression/phosphorylation of STAT3 and reduced expression of STAT3-dependent molecules including suppressor of cytokine signalling 3, CCL-2, and ICAM-1 in cultured GCA-involved arteries and patients’ peripheral blood mononuclear cells (PBMCs). A similar trend was observed in aortic tissue. Consistently, tocilizumab reduced PBMC adhesiveness to vascular smooth muscle cells and human umbilical vein endothelial cells and chemotaxis towards supernatants of tocilizumab-treated GCA arteries. In some specimens, tocilizumab increased STAT1 phosphorylation and expression of STAT1-dependent chemokines including CXCL9 and CXCL10. Conclusions Tocilizumab has a significant impact on vascular lesions by reducing, but not abrogating, key molecules involved in PBMC recruitment. About half of the patients may activate alternative inflammatory pathways i

关键词： Rh血型   抗原   检验   精准输血   输血安全  

摘要： 目的 对Rh血型D、C、E抗原的分布和其临床应用情况进行分析。方法 收集近5年(2020年3月—2025年3月)因上消化道出血、失血性休克等原因需多次输血治疗的55例病例资料,均完成RhD的血型检测,研究组为符合Rh相容性输血优先Ⅰ级和Ⅱ级,对照组为符合优先Ⅲ级和交叉配血随机盲配,分别是25例、30例。采用抗人球蛋白试验进行抗体筛查,比较两组血红蛋白、红细胞比容差异。结果 55例病例的血液标本Rh血型D、C、E抗原检测:D抗原阳性占比98.18%、C抗原阳性占比94.55%、E抗原阳性占比49.09%;输血前,两组的血红蛋白水平、红细胞比容无显著差异(P>0.05);输血后,研究组的血红蛋白、红细胞比容高于对照组(P<0.05)。对照组血红蛋白尿、腰背疼痛发生率要显著高于研究组(P<0.05)。结论 根据对输血者Rh血型D、C、E抗原的检测为其提供相同血型抗原血液,能保证输血治疗有效性及安全性。

关键词： IL-1 alpha   iNOS   macrophages   obesity   Th17 cells   tuberculosis  

摘要： IL-1 alpha, IL-1 beta, IFN-gamma, IL-17 and the expression of inducible nitric oxide synthase (iNOS) enzyme by macrophages, which generate nitric oxide, are protective against tuberculosis, a disease caused by Mycobacterium tuberculosis. The severity of tuberculosis can be dependent on bacterial load and/or lung immunopathology. Tuberculosis is aggravated by existing comorbidities such as obesity. Obesity induces metabolic dysfunction, meta inflammation and dysbiosis, which increase the prevalence of respiratory diseases and worsen immunopathology. The deficiency of IL-1 alpha (IL-1 alpha-/-) induces deleterious lung monocytic inflammation and functional activation of the adaptive immune response mediated by T cells during M. tuberculosis infection in non-obese mice. Although iNOS and IFN-gamma have been described as protective in experimental tuberculosis, using a model of obesity induced by high-fat diet, we show here an increase in iNOS-expressing interstitial macrophages positively correlated with M. tuberculosis numbers in the lungs of IL-1 alpha-/- animals, followed by increased frequency of IFN-gamma and decreased frequency of IL-17-producing T cells, showing that IFN-gamma and iNOS contribute to immunopathology and pulmonary damage. The protective effect of IL-1 alpha, characterised by reduction of lung immunopathology, is dependent on IL-17-producing CD4+ cells that negatively regulate iNOS expression on macrophages. Our data provide important implications for tuberculosis with existing obesity that aggravates lung immunopathology associated with an exacerbation of IFN-gamma-producing and iNOS-expressing cells.