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【目的】定位并注释双峰驼主要组织相容性复合体(major histocompatibility complex,MHC)基因序列,为进一步研究双峰驼MHC基因提供科学依据。【方法】运用比较基因组学方法,提取人类MHC(HLA)基因编码序列和牛MHC(BoLA)基因编码序列并分别与双峰驼转录本进行blastn基因序列比对,识别出相似度较高的scaffolds,通过分析HLA、BoLA基因序列比对在这些scaffolds上的位置顺序,对多条scaffolds进行拼接,得到双峰驼MHC的Pseudo chromosome;再分别提取HLA、BoLA全基因组序列与双峰驼已拼接的scaffolds进行基因组共线性分析,利用lastz建立起的Pseudo chromosome与HLA、BoLA全基因组序列的线性关系判断筛选出的scaffolds是否准确;然后通过分析MHC基因在两物种间的线性关系,在双峰驼参考基因组中提取出MHC基因序列,并对这些序列进行基因注释;最后根据得到的双峰驼MHC基因绘制系统进化树,研究其基因间的进化关系。【结果】通过对HLA、BoLA基因编码序列与双峰驼转录本用blastn进行序列比对,识别出了相似度较高的3条scaffolds,即NW_011511766.1(全长4.1M)、NW_011515227.1(全长1.2M)和NW_011514613.1(全长15K),对其拼接得到双峰驼MHC的Pseudo chromosome;利用lastz共线性分析,识别出HLA基因序列和BoLA基因序列并比对出其在双峰驼MHC基因的共线性区域。该区域与拼接得到的Pseudo chromosome一致,证明筛选出的scaffolds是准确的。并且发现Class-Ⅰ类和Class-Ⅲ类基因集中分布在NW_011515227.1上,而Class-Ⅱ类基因集中分布在NW_011511766.1和NW_011514613.1上,进一步分析得知Class-Ⅱ类基因主要分布在NW_011511766.1的3.5—4.1M的位置;将存在共线性区域的序列提取出来,与比对到双峰驼上的MHC基因的编码序列进行blat分析,结果在双峰驼基因组中共识别出24个与牛BoLA基因高度相似的基因,其中Ⅰ类基因1个,Ⅱ类10个,Ⅲ类基因13个。对双峰驼这24个MHC基因进行信息注释并绘制系统进化树,结果显示注释的Class-Ⅰ类和Class-Ⅱ类基因在同一分支。【结论】通过比较基因组学方法定位并注释了双峰驼的MHC基因,将双峰驼MHC基因序列定位到了3条scaffolds上,找到并注释了24个MHC基因,绘制了双峰驼MHC的Pseudo chromosome,为进一步研究双峰驼MHC基因奠定了理论基础。  相似文献   
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[目的]对结核分枝杆菌RD1区T细胞表位分布情况进行预测和分析。[方法]利用NetMHC server生物信息学软件,以和HLA-Ⅱ和HLAⅠ-类分子结合能力为指标,分别对结核分枝杆菌RD1区9个编码蛋白进行T细胞抗原表位预测。[结果]通过预测,共获得和HLA-Ⅱ类分子结合的抗原表位1 580个和HLA-Ⅰ类分子结合的抗原表位336个。[结论]预测获得的T细胞抗原表位将对结核病特异性检测及新的结核疫苗研发起到借鉴作用。  相似文献   
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AIM: To investigate the association between HBV infection and HLA-DPB1 gene in population of Guangzhou Chinese. METHODS: 58 unrelated patients (test positive of HbsAg, HBeAg, HbcAb) and 75 unrelated healthy control individuals were typed by sequencing based typing (SBT) method in their HLA-DPB1 gene. RESULTS: The phenotype frequencies of HLA-DPB1 alleles of patients and control have no significant difference. CONCLUSION: These results indicate that there is no association between HLA-DPB1 gene and HBV infection.  相似文献   
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Toxocara canis is regarded as the main cause of human toxocarosis but the relative contribution of T. cati is probably underestimated; serological and other diagnostic methods used in most studies of this zoonotic disease do not distinguish between the two parasites. The definitive hosts for T. canis are caniidae. Pups generally have higher infection rates than adult animals and are a major source of eggs in the environment. Humans usually acquire T. canis infection by accidental ingestion of embryonated eggs or encapsulated larvae from the environment or contaminated food, such infections may lead to visceral larva migrans (VLM), ocular larva migrans (OLM) or covert toxocarosis (CT). Although a mixed Th1- and Th2-mediated immunological response, particularly with high levels of IgE and eosinophilia is observed, the underlying mechanisms of molecular and immunopathogenesis for the development of the symptomatic syndromes of VLM, OLM, or of asymptomatic CT are largely unclear. Studies have indicated that immunological defences against various infectious diseases may be highly influenced by complex interactions of environmental and host genetic factors e.g. MHC class I and II, also known as human leucocyte antigen (HLA). Toxocara spp. infections are associated with a polarized CD4+ Th2 response with high IgE levels and eosinophilia, mediated mainly by HLA class II molecules. Associations have been made between HLA class II and pathological severity and host genetic effects on exposure to infection. Recent research suggests Foxp3+ CD4+CD25+-expressing T regulatory (Treg) cells play a role in regulation of the immunopathology of granulomas in experimental toxocaral granulomatous hepatitis and in enhanced expression of TGF-β1, which is an important factor for the local survival and function of Treg observed during T. canis invasion in the mouse small intestine, liver, muscle, and brain. Since the potential susceptibility loci HLA class II molecules, are considered involved in the regulation of a Th2-dominant immunity which is highly controlled by Foxp3+ CD4+CD25+ Treg cells by stimulation through TGF-β1, which thus provides a beneficial environment to T. canis larvae but severe injuries to local organs. However, TGF-β1 variant Leu10Pro known to be involved in disease severity warrants further elucidation as this too may have a role in the severity of human toxocarosis. Exploration of TGF-β1 polymorphism, Foxp3+ CD4+CD25+ Treg cells, and MHC polymorphisms may allow insight into the contribution made by environmental and genetic factors in influencing disease syndrome type and severity in humans with toxocarosis.  相似文献   
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