Clark David A, Dmetrichuk Jennifer M, McCready Elizabeth, Dhesy-Thind Sukhbinder, Arredondo Jorge L
Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.
Am J Reprod Immunol. 2017 Jul;78(1). doi: 10.1111/aji.12665. Epub 2017 Mar 22.
Expression of CD200 at the feto-maternal interface is associated with successful murine and human pregnancy. CD200 binding to CD200 receptors on lymphomyeloid cells suppresses inflammation and induces Tregs. CD200 receptors are also expressed on mouse and human placental trophoblast cells. What is the expression of CD200 and CD200R in human missed abortions which have preserved Treg levels and in chronic histiocytic intervillositis (CHI) where maternal inflammatory cells cause IUGR?
Immunohistiochemistry for CD200, CD200R, and Ki67 using human placental sections from missed abortions, term placenta, and CHI. PCR testing was done for trisomy in missed abortion.
CD200 and CD200R were expressed by human villus trophoblasts from 2 weeks post-implantation to term. Cytotrophoblast proliferation (Ki-67 count) decreased at term. In first trimester missed abortion cases, CD200>CD200R villus trophoblasts accompanied missed abortion of non-trisomic male fetuses. CD200 and Ki67 trophoblast proliferation was preserved in CHI with maternal inflammatory cell infiltration but CD200R was greatly decreased.
Residual CD200 activity may prevent completion of abortions via induction of Treg cells. In CHI, infiltrating maternal effector T cells may block Treg induction. An autocrine role for CD200-CD200R interaction versus inhibition of soluble CD200 by soluble CD200R is discussed.
胎儿-母体界面处CD200的表达与小鼠和人类的成功妊娠相关。CD200与淋巴髓样细胞上的CD200受体结合可抑制炎症并诱导调节性T细胞（Tregs）。CD200受体也表达于小鼠和人类胎盘滋养层细胞上。在保留了Treg水平的人类稽留流产以及母体炎症细胞导致胎儿生长受限（IUGR）的慢性组织细胞绒毛间炎（CHI）中，CD200和CD200R的表达情况如何？
使用来自稽留流产、足月胎盘和CHI的人胎盘切片，对CD200、CD200R和Ki67进行免疫组织化学检测。对稽留流产进行三体性的聚合酶链反应（PCR）检测。
从着床后2周直至足月，人绒毛滋养层细胞均表达CD200和CD200R。足月时细胞滋养层细胞增殖（Ki-67计数）下降。在孕早期稽留流产病例中，CD200>CD200R的绒毛滋养层细胞伴随着非三体性男性胎儿的稽留流产。在有母体炎症细胞浸润的CHI中，CD200和Ki67的滋养层细胞增殖得以保留，但CD被大大降低。
残余的CD200活性可能通过诱导Treg细胞来阻止流产的完成。在CHI中，浸润的母体效应T细胞可能会阻断Treg的诱导。文中讨论了CD200-CD200R相互作用的自分泌作用与可溶性CD200R对可溶性CD200的抑制作用。 200R
