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PLoS Pathog:轮状病毒感染或可增加个体患I型糖尿病的风险

  1. I型糖尿病
  2. PLoS Pathog
  3. 感染
  4. 轮状病毒

来源:生物谷 2014-04-01 23:39

近日,来自墨尔本大学的研究人员通过研究表明,引发儿童严重腹泻的罪魁祸首—轮状病毒可以加速小鼠患I型糖尿病,相关研究成果刊登于国际杂志PLoS Pathogens上。该研究或为探究轮状病毒感染引发小鼠患自身免疫疾病提供了研究依据,同时也为揭示轮状病毒感染的机制提供了一定思路。

2014年4月1日 讯 /生物谷BIOON/ --近日,来自墨尔本大学的研究人员通过研究表明,引发儿童严重腹泻的罪魁祸首——轮状病毒可以加速小鼠患I型糖尿病,相关研究成果刊登于国际杂志PLoS Pathogens上。该研究或为探究轮状病毒感染引发小鼠患自身免疫疾病提供了研究依据,同时也为揭示轮状病毒感染的机制提供了一定思路。

研究者Barbara Coulson表示,轮状病毒感染加速I型糖尿病发生或许是一种“旁观者效应”,这也就表明轮状病毒可以引发免疫系统的强烈激活,当免疫系统激活超过阈值就会不仅攻击轮状病毒,而且还会攻击机体自身的细胞,比如攻击胰岛素产生细胞。这项研究也是研究者首次发现轮状病毒可以激活小鼠的机体免疫应答。

研究者表示,这种“旁观者效应”机制为理解因轮状病毒感染而引发的I型糖尿病的发病机制提供了一定的研究思路;当然在人类机体中也存在轮状病毒感染,而且轮状病毒感染也会引发儿童出现I型糖尿病,未来还需要更为深入的研究来揭示其中的机制。

理解轮状病毒感染影响人类I型糖尿病的发育的机制对于开发抑制儿童感染轮状病毒的策略和疗法提供了很好的研究数据;研究者指出,降低由轮状病毒引发的免疫反应的疗法或许对于治疗患者的I型糖尿病会很有帮助。(生物谷Bioon.com)

doi:10.1371/journal.ppat.1003998
Rotavirus Activates Lymphocytes from Non-Obese Diabetic Mice by Triggering Toll-Like Receptor 7 Signaling and Interferon Production in Plasmacytoid Dendritic Cells

Pane JA, Webster NL, Coulson BS

It has been proposed that rotavirus infection promotes the progression of genetically-predisposed children to type 1 diabetes, a chronic autoimmune disease marked by infiltration of activated lymphocytes into pancreatic islets. Non-obese diabetic (NOD) mice provide a model for the human disease. Infection of adult NOD mice with rhesus monkey rotavirus (RRV) accelerates diabetes onset, without evidence of pancreatic infection. Rather, RRV spreads to the pancreatic and mesenteric lymph nodes where its association with antigen-presenting cells, including dendritic cells, induces cellular maturation. RRV infection increases levels of the class I major histocompatibility complex on B cells and proinflammatory cytokine expression by T cells at these sites. In autoimmunity-resistant mice and human mononuclear cells from blood, rotavirus-exposed plasmacytoid dendritic cells contribute to bystander polyclonal B cell activation through type I interferon expression. Here we tested the hypothesis that rotavirus induces bystander activation of lymphocytes from NOD mice by provoking dendritic cell activation and proinflammatory cytokine secretion. NOD mouse splenocytes were stimulated with rotavirus and assessed for activation by flow cytometry. This stimulation activated antigen-presenting cells and B cells independently of virus strain and replicative ability. Instead, activation depended on virus dose and was prevented by blockade of virus decapsidation, inhibition of endosomal acidification and interference with signaling through Toll-like receptor 7 and the type I interferon receptor. Plasmacytoid dendritic cells were more efficiently activated than conventional dendritic cells by RRV, and contributed to the activation of B and T cells, including islet-autoreactive CD8+ T cells. Thus, a double-stranded RNA virus can induce Toll-like receptor 7 signaling, resulting in lymphocyte activation. Our findings suggest that bystander activation mediated by type I interferon contributes to the lymphocyte activation observed following RRV infection of NOD mice, and may play a role in diabetes acceleration by rotavirus.

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