Huddleston Heather, Schust Danny J
Division of Reproductive Endocrinology and Fertility, Department of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Am J Reprod Immunol. 2004 Apr;51(4):283-9. doi: 10.1111/j.1600-0897.2004.00157.x.
Viruses and fetuses face similar immunologic challenges. Each must evade immune detection and destruction. The virus must avoid host recognition of intracellular infection; the fetus allogenic recognition. Each has manipulated the process of antigen presentation to allow survival in an immunologic environment otherwise predictably hostile. How have these approaches co-evolved? What can they teach us about viral pathogenesis and immunologic interactions at the maternal-fetal interface?
Review of relevant literature.
Special classical and non-classical MHC class I products are spared from downregulation in the placenta and from viral immunoevasive strategies.
Viruses rely upon some of the same strategies to avoid immune detection as do trophoblast cells. In the future, viral infections may prove a useful tool for studies of immunology at the maternal-fetal interface.
病毒和胎儿面临相似的免疫挑战。两者都必须逃避免疫检测和破坏。病毒必须避免宿主识别细胞内感染;胎儿则要避免同种异体识别。它们都操控了抗原呈递过程,以便在原本可预测为敌对的免疫环境中存活。这些方法是如何共同进化的?它们能在母胎界面的病毒发病机制和免疫相互作用方面给我们带来什么启示?
对相关文献进行综述。
特殊的经典和非经典MHC I类产物在胎盘中不会被下调,也不受病毒免疫逃避策略的影响。
病毒采用了一些与滋养层细胞相同的策略来避免免疫检测。未来,病毒感染可能会被证明是研究母胎界面免疫学的有用工具。