Biotechnology Essay代写;IV流感病毒

Keywords:Biotechnology Essay代写

流感病毒（IV）是高度传染性的单链RNA病毒家族的Orthomyxoviridae，其基因组由八个不同的RNA片段编码的蛋白（诺伊曼等人11-12。2004；麦地那等。2011）。季节性流感（如流感病毒fl，H3N2）导致每年流行可导致免疫功能低下的人严重的疾病，包括年轻人和老年人（伤害等。2012；rappupli等人。2012）。宿主细胞因子的免疫反应提供了第一道防线，对fl流感病毒（IAV）感染（Teijaro等人。2011）。研究还表明，流感病毒感染诱导过量的细胞因子的产生（细胞因子风暴）和白细胞被认为是人类严重疾病的主要贡献者强大的招聘（厄尔等人。2010；岩崎等人。2011）。然而，机制的细胞因子诱导的增加在IAV感染迄今为止在很大程度上还不清楚。 白介素-22（IL-22）是IL-10家族成员，由CD4+ T辅助细胞17（Th17）产生的细胞，自然杀伤（NK）细胞CD11c+髓系细胞和淋巴组织诱导（LTI）细胞（鲁茨等人。2013；塞拉等人。2009）。IL-22受体是由IL-22R1和IL-10R2亚基和在非造血起源于皮肤、肾、肝、肺细胞发现，肠道（Wolk等。2004；欧阳等。2008）。IL-22在自身免疫性和炎症中起着fl疾病的双重作用。在实验性的系统，其对肝细胞和屏障表面上皮细胞有保护作用（澳佳等人。2008；郑等。2008）。另一方面，不受控制的IL-22参与炎症性疾病如牛皮癣、红斑狼疮、类风湿性关节炎（Van等人。2012；张等。2007）。 白介素-34（IL-34）是最近发现的一种细胞因子，已由一个分泌蛋白库功能筛选鉴定（林等人。2008；梅兰妮等。2012）。发病的特定fi脾组织上表达，主要在红髓区，并支持人类单核细胞的存活率，促进巨噬细胞集落形成单位（CFU-GM）形成在人类骨髓细胞培养（Chemel等人。2012；Hwang等。2012）。发病是一个二聚体糖蛋白呈现不同的氨基酸序列与集落刺激因子1（CSF-1）（baud'huin等人。2010）。小鼠发病也促进腹腔巨噬细胞的生存和骨髓祖细胞的增殖（王等人。2012；戴等。2002）。虽然发病中已经描述了几个功能，在炎症网络IL-34明确作用尚未确定

Biotechnology Essay代写;IV流感病毒

uenza viruses (IV) are highly contagious single-stranded RNA viruses in the Orthomyxoviridae family and its genome consists of eight distinct RNA segments which encode 11-12 proteins (Neumann et al. 2004; Medina et al. 2011). Seasonal strains (e.g. Influenza A viruses, H3N2) that cause annual epidemics can cause severe disease in immunocompromised individuals, including the young and the elderly (Hurt et al. 2012; Rappupli et al. 2012). The host cytokine immune response provides the first line of defense against Influenza A viruses (IAV) infection (Teijaro et al. 2011). Studies have also shown that IAV infection induces excessive cytokine production (Cytokine storm) and robust recruitment of leukocytes which are hypothesized to be major contributors to severe disease in humans (Jewell et al. 2010; Iwasaki et al. 2011). However, the mechanisms underlying the increased induction of cytokines during IAV infection have to date been largely unclear.
Interleukin-22 (IL-22) is a member of the IL-10 family and produced by CD4+ T helper 17 (Th17) cells, natural killer (NK) cells, CD11c+ myeloid cells, and lymphoid tissue inducer-like (LTi) cells (Rutz et al. 2013; Cella et al. 2009). The IL-22 receptor is composed of the IL-22R1 and IL-10R2 subunits and is found on cells of nonhematopoietic origin in the skin, kidney, liver, lung, and gut (Wolk et al. 2004; Ouyang et al. 2008). IL-22 plays a dual role in autoimmune and inflammatory diseases. In experimental noninfectious systems, IL-22 exerts a potent protective effect on hepatocytes and epithelial cells at barrier surfaces (Aujia et al. 2008; Zheng et al. 2008). On the other hand, uncontrolled IL-22 involved in the inflammatory disorders such as psoriasis, lupus erythematosus, and rheumatoid arthritis (Van et al. 2012; Zhang et al. 2007).
Interleukin-34 (IL-34) is a recently discovered cytokine and has been identified by functional screening of a library of secreted proteins (Lin et al. 2008; Melanie et al. 2012). IL-34 is specifically expressed in splenic tissues, predominantly in the red pulp region, and supported human monocyte survival and to promote the formation of the colony-forming unit-macrophage (CFU-M) in human bone marrow cell cultures (Chemel et al. 2012; Hwang et al. 2012). IL-34 is a dimeric glycoprotein which presents different amino acid sequence with colony-stimulating factor 1 (CSF-1) (Baud’huin et al. 2010). Murine IL-34 also promotes peritoneal macrophages survival and bone marrow progenitor cell proliferation (Wang et al. 2012; Dai et al. 2002). Although several functions of IL-34 have been described, a clear role for IL-34 in inflammatory network has not been established.