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西尼罗河病毒在γ干扰素难治性早期小鼠滋养层细胞上诱导I类主要组织相容性复合体抗原表达。

Induction of class I major histocompatibility complex antigen expression by West Nile virus on gamma interferon-refractory early murine trophoblast cells.

作者信息

King N J, Maxwell L E, Kesson A M

机构信息

Department of Microbiology, John Curtin School of Medical Research, Australian National University, Canberra.

出版信息

Proc Natl Acad Sci U S A. 1989 Feb;86(3):911-5. doi: 10.1073/pnas.86.3.911.

Abstract

Primary murine trophoblast giant cells (TGC) do not express detectable major histocompatibility complex (MHC) antigens and are refractory to the MHC-increasing effects of alpha and beta (virus-induced) interferons and gamma (immune type) interferon during early implantation (postcoital days 3.5-6). West Nile virus infection of primary TGC monolayers from postcoital-day-3.5 preimplantation blastocysts induced paternal MHC antigen expression within 16 hr, as detected by immunogold labeling for electron microscopy. Induction is unlikely to have been mediated by secreted virus-induced interferons or other factors, as it occurred in the presence of high concentrations of anti-alpha/beta interferon antibodies and was not induced by virus-inactivated supernatants from MHC-induced primary TGC cultures. Attempts to induce MHC antigen expression with poly(I.C) or recombinant tumor necrosis factor alpha in primary TGC cultures also failed. Thus, the apparent inhibition of MHC antigen expression in primary TGC during early implantation and their refractoriness to induction of de novo MHC antigen expression is not absolute. This may represent a maternal-and/or species-protective evolutionary device. As such, manipulation of this phenomenon may allow a conclusive assessment of the significance of inhibition of MHC antigen expression on trophoblast cells in the implanting semiallogeneic embryo.

摘要

原代小鼠滋养层巨细胞(TGC)不表达可检测到的主要组织相容性复合体(MHC)抗原,并且在植入早期(交配后第3.5 - 6天)对α和β(病毒诱导的)干扰素以及γ(免疫型)干扰素增加MHC的作用具有抗性。通过免疫金标记电子显微镜检测发现,来自交配后第3.5天着床前胚泡的原代TGC单层细胞感染西尼罗河病毒后,在16小时内诱导了父本MHC抗原表达。诱导不太可能是由分泌的病毒诱导干扰素或其他因子介导的,因为它发生在高浓度抗α/β干扰素抗体存在的情况下,并且未被来自MHC诱导的原代TGC培养物的病毒灭活上清液诱导。在原代TGC培养物中用聚肌胞苷酸(poly(I.C))或重组肿瘤坏死因子α诱导MHC抗原表达的尝试也失败了。因此,早期植入期间原代TGC中MHC抗原表达的明显抑制以及它们对从头诱导MHC抗原表达的抗性并非绝对。这可能代表了一种母体和/或物种保护的进化机制。因此,对这一现象的操纵可能有助于最终评估植入半同种异体胚胎中滋养层细胞MHC抗原表达抑制的意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf5a/286588/dd722905095b/pnas00243-0166-a.jpg

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