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1.
XGD-1对人外周血T淋巴细胞增殖和IL-2R表达的影响   总被引:1,自引:1,他引:0  
目的 探讨XGD—l的免疫抑制作用及其作用机理。方法 不同浓度的XGD—l作用于植物血凝索(PHA)和刀豆索A(ConA)诱导的正常人外周血T淋巴细胞,共同培养48h和72h,用改良MTT法观察XGD—l对人T淋巴细胞增殖的影响,用流式细胞术检测XGD—l对T淋巴细胞表面IL—2R表达的影响;同时观察联合应用CsA和XGD—l对细胞增殖及IL—2R表达的影响。结果 XGD—l对PHA和ConA诱导的正常人外周血T淋巴细胞增殖有明显的抑制作用,其作用与药物浓度有关,在一定剂量范围内,抑制作用随XGD—l剂量的递增而加强;XGD—l对PHA和ConA激活的T淋巴细胞表面IL-2R的表达有显著抑制作用,阳性率从正常对照活化细胞的47.67%降为25.03%;联合应用CsA,上述抑制作用增强。结论 XGD-l具有免疫抑制作用,能降低IL-2R表达,可能是其免疫抑制作用的重要机理之一。  相似文献   
2.
To elucidate the possible involvement of the inducible nitric oxide synthase (iNOS) and NO in the development of lymphocytic choriomeningitis (LCM), the consequences of inhibition of iNOS by the inhibitor aminoguanidine was examined in mice following intracerebral infection with LCM virus (LCMV). Aminoguanidine administration to mice infected with LCMV completely blocked increased plasma nitrate/nitrite levels and led to increased proinflammatory cytokine gene expression at early stages of lesion development in the brain, enhanced clinical severity and decreased survival time. The levels of LCMV recovered from the brain of aminoguanidine treated mice did not differ from those in infected control mice. These findings argue against either an anti-viral or pathogenic role of NO in LCM but rather suggest a possible protective action of this mediator.  相似文献   
3.
Collagenous,microscopic and lymphocytic colitis. An evolving concept   总被引:4,自引:0,他引:4  
Collagenous colitis and lymphocytic colitis (previously described as microscopic colitis) are two newly recognised forms of colitis. Both have generated much controversy and continue to do so; their aetiology and pathogenesis are unresolved and their association with a variety of immune-related disorders is intriguing. Response to available therapeutic modalities is often disappointing. The possible relationship or overlap between these two conditions remains a controversial issue. The aim of this review is essentially to present an overview of collagenous colitis and lymphocytic colitis and to propose an unifying concept with an adapted terminology.  相似文献   
4.
再生障碍性贫血患者淋巴细胞表型变化   总被引:7,自引:0,他引:7  
目的:研究再生障碍性贫血(AA)患者骨髓(BM)及外周血(PB)淋巴细胞及其活化相关分子的表达及临床意义。方法:采用单色和双色免疫荧光标记法,流式细胞仪分析AA患者的BM和PB中淋巴细胞膜分子的表达。结果:AA患者BM和BP中CD8^ 细胞增加,CD4/CD8比例下降,BM在CD25^ 细胞和HLA-DR^ 细胞增多,急性AA增加尤为显著(P<0.01),BM中CD16^ 或CD56^ 细胞也明显增多(P<0.05),双标记分析提示T细胞主要为CD8^ 细胞:急性AA患者CD8^ -CD25^ 细胞显著增多(P<0.01),AA患者BM中淋巴细胞活化相关分子表达增多,尤其4-1BB^ ,CD95L^ 和CD40L+细胞显著增多(P<0.01),结论:AA患者BM中淋巴细胞活化相关膜分子增多,是AA免疫功能异常及最终导致造血功能衰竭的原因之一。  相似文献   
5.
This report describes a case of lymphocytic hypophysitis in a 63-year-old man who presented with symptoms of a pituitary mass lesion associated with hypothyroidism and hypogonadism. Postoperative endocrinological testing demonstrated gonadotropic, thyrotropic, and corticotropic hypopituitarism, and the patient was commenced on replacement therapy with hydrocortisone and levothyroxine. Histological examination of the pituitary tissue obtained by transsphenoidal surgery revealed lymphocytic hypophysitis without evidence of a pituitary adenoma. The vast majority of patients with lymphocytic hypophysitis are women particularly during pregnancy and the puerperium. Until recently only four men were reported in the literature. The pathogenesis of lymphocytic hypophysitis is uncertain but autoimmune mechanisms are possibly involved.  相似文献   
6.
This study assessed the morphological criteria for the diagnosis of various types of lymphocytic thyroiditis in fine-needle aspirates. Of 950 aspirates, 121 revealed lymphocytic thyroiditis, including Hashimoto's thyroiditis (partly confirmed by serological or histological examination) and focal thyroiditis adjacent to neoplasms. The diagnosis of Hashimoto's thyroiditis was easy when the aspirated material was adequate and contained oxyphilic cells; in the fibrous type, diagnosis was rather difficult. Focal thyroiditis may be confused with Hashimoto's thyroiditis, especially when adjacent to neoplasm. Surgical exploration should be performed in cases of severe lymphocytic thyroiditis revealed by fine-needle aspiration with repeatedly negative antibody titers in order to exclude neoplasm.  相似文献   
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Interstitial lung disease (ILD) in children (chILD) is a heterogeneous group of rare respiratory disorders that are mostly chronic and associated with high morbidity and mortality. The pathogenesis of the various chILD is complex and the diseases share common features of inflammatory and fibrotic changes of the lung parenchyma that impair gas exchanges. The etiologies of chILD are numerous. In this review, we chose to classify them as ILD related to exposure/environment insults, ILD related to systemic and immunological diseases, ILD related to primary lung parenchyma dysfunctions and ILD specific to infancy. A growing part of the etiologic spectrum of chILD is being attributed to molecular defects. Currently, the main genetic mutations associated with chILD are identified in the surfactant genes SFTPA1, SFTPA2, SFTPB, SFTPC, ABCA3 and NKX2-1. Other genetic contributors include mutations in MARS, CSF2RA and CSF2RB in pulmonary alveolar proteinosis, and mutations in TMEM173 and COPA in specific auto-inflammatory forms of chILD. However, only few genotype-phenotype correlations could be identified so far. Herein, information is provided about the clinical presentation and the diagnosis approach of chILD. Despite improvements in patient management, the therapeutic strategies are still relying mostly on corticosteroids although specific therapies are emerging. Larger longitudinal cohorts of patients are being gathered through ongoing international collaborations to improve disease knowledge and targeted therapies. Thus, it is expected that children with ILD will be able to reach the adulthood transition in a better condition.  相似文献   
10.
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