近日，国际著名杂志PNAS在线刊登了国外研究人员的最新研究成果“Murine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity，”，文章中，科研人员报告说，长期感染一种鼠科疱疹病毒能防止小鼠出现狼疮样自体免疫疾病。
尽管此前的报告把导致人类单核细胞增多症的Epstein Barr病毒（EBV）与诸如狼疮等自体免疫疾病的发病联系起来，几乎没有感染病毒的个体出现自体免疫疾病。Philippa Marrack及其同事们研究了狼疮和γ疱疹病毒68—一种Epstein Barr病毒（EBV）样小鼠病毒，能在小鼠身上产生单核细胞增多症样的症状—之间的联系。这组作者报告说，长期感染这种病毒阻断了易出现狼疮样疾病的雌性小鼠的与狼疮有关的自体免疫抗体的产生。
在感染后的至多一年时间里，雄性和雌性的易感狼疮的小鼠—它们都表现出了被激活的B细胞、T细胞和树突状细胞的数量减少—看上去得到了保护，没有出现狼疮样疾病。已知狼疮样疾病会因为这些免疫细胞的激活而恶化。此外，长期感染γ疱疹病毒68能抑制肾脏的炎症和组织损伤，这提示这种病毒防止了—但没有引发或使之恶化—小鼠的自体免疫。这些发现提出了一种可能性，即γ疱疹病毒—诸如Epstein Barr病毒（EBV）—可能保护某些人免于出现自体免疫疾病。（生物谷Bioon.com）
doi:10.1073/pnas.1203019109
PMC:
PMID:
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.
