近日,，國際著名雜志PNAS在線刊登了國外研究人員的最新研究成果“Murine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity,，”，文章中,，科研人員報告說,，長期感染一種鼠科皰疹病毒能防止小鼠出現(xiàn)狼瘡樣自體免疫疾病。
盡管此前的報告把導(dǎo)致人類單核細(xì)胞增多癥的Epstein Barr病毒（EBV）與諸如狼瘡等自體免疫疾病的發(fā)病聯(lián)系起來,，幾乎沒有感染病毒的個體出現(xiàn)自體免疫疾病,。Philippa Marrack及其同事們研究了狼瘡和γ皰疹病毒68—一種Epstein Barr病毒（EBV）樣小鼠病毒，能在小鼠身上產(chǎn)生單核細(xì)胞增多癥樣的癥狀—之間的聯(lián)系,。這組作者報告說,，長期感染這種病毒阻斷了易出現(xiàn)狼瘡樣疾病的雌性小鼠的與狼瘡有關(guān)的自體免疫抗體的產(chǎn)生。
在感染后的至多一年時間里,，雄性和雌性的易感狼瘡的小鼠—它們都表現(xiàn)出了被激活的B細(xì)胞,、T細(xì)胞和樹突狀細(xì)胞的數(shù)量減少—看上去得到了保護(hù),，沒有出現(xiàn)狼瘡樣疾病。已知狼瘡樣疾病會因?yàn)檫@些免疫細(xì)胞的激活而惡化,。此外,，長期感染γ皰疹病毒68能抑制腎臟的炎癥和組織損傷，這提示這種病毒防止了—但沒有引發(fā)或使之惡化—小鼠的自體免疫,。這些發(fā)現(xiàn)提出了一種可能性,，即γ皰疹病毒—諸如Epstein Barr病毒（EBV）—可能保護(hù)某些人免于出現(xiàn)自體免疫疾病。（生物谷Bioon.com）
doi:10.1073/pnas.1203019109
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Murine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity
Jennifer D. Larsona, Joshua M. Thurmanb, Anatoly V. Rubtsova,c, David Claypoold, Philippa Marracka,c,1, Linda F. van Dyka,d, Raul M. Torresa, and Roberta Pelandaa,1
Gammaherpesvirus infections, such as those caused by EBV, have been suggested to promote the development of autoimmunity. To test this idea, we infected healthy WT and lupus-prone B6.Sle123 mice with an EBV-related and rodent-specific gammaherpesvirus, γHV68. Although acute γHV68 infection increased autoantibody levels for 4 to 6 wk, latent infection inhibited these responses for 1 y. The inhibition of autoantibody expression was only observed in B6.Sle123 females and not in males, which already displayed lower autoantibody titers. Contrary to the initial hypothesis, infection of young B6.Sle123 mice, both male and female, resulted in suppression of lymphoid activation and expansion and of glomerular inflammation and sclerosis, preserving kidney function. Moreover, γHV68 infection led to reduced autoantibody titers, lymphoid activation, and glomerular inflammation whether lupus-prone females were infected before or during disease manifestation. Finally, γHV68 infection also inhibited autoantibody production in the genetically distinct MRL/lpr lupus-prone mice. Our findings indicate that γHV68 infection strongly inhibits the development and progression of lupus-like disease in mice that spontaneously develop this condition mediating its beneficial effects at the humoral, cellular, and organ levels. The mechanisms by which the virus exerts this down-modulatory action are not yet clear, but appear to operate via reduced activation of dendritic cells, T cells, and B cells. Gammaherpesviruses coevolved with the vertebrate immune systems, establishing lifelong infections in humans and other mammals. Our findings that γHV68 infection prevents rather than exacerbates autoimmunity in mice suggest that infection with gammaherpesviruses may be protective rather than pathological in most individuals.
