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孕期抗自身红细胞斑块形成细胞。免疫调节变化的一个参数。

Anti-autologous erythrocyte plaque-forming cells in pregnancy. A parameter of immunoregulatory change.

作者信息

Koros A M, Hamill E C, Depp O R

出版信息

Vox Sang. 1978;35(5):277-87. doi: 10.1111/j.1423-0410.1978.tb02936.x.

DOI:10.1111/j.1423-0410.1978.tb02936.x
PMID:567889
Abstract

Peripheral blood leukocytes (PBL) from 16 persons (6 Rh-sensitized pregnant women, 1 pregnant non-Rh-sensitized woman, 3 nonpregnant non-Rh-sensitized women, and 6 non-Rh-sensitized males) were assayed for plaque-forming cells (PFC) against several erythrocyte targets. 6 of 7 pregnant women had PFC, whereas only 1 of 6 males had PFC to autologous red cells. Antiautologous erythrocyte PFC in all of the pregnant Rh-sensitized women as well as the 1 nonpregnant multiparous woman may be the result of alloimmunization of mothers by their fetuses during gestation. Further studies in this area would be valuable in determining not only the immune status of a mother in relation to her fetus, but also would be of value in determining the consequences of that immune status on both mother and fetus. Such information would also provide a further clue to the etiology of autoimmune disease.

摘要

对16人的外周血白细胞(PBL)(6名Rh致敏孕妇、1名未致敏的孕妇、3名未致敏的非孕妇和6名未致敏的男性)进行检测,以测定针对几种红细胞靶标的空斑形成细胞(PFC)。7名孕妇中有6名有PFC,而6名男性中只有1名对自身红细胞有PFC。所有Rh致敏孕妇以及1名未孕经产妇的抗自身红细胞PFC可能是母亲在妊娠期被胎儿同种免疫的结果。该领域的进一步研究不仅对于确定母亲相对于其胎儿的免疫状态具有重要价值,而且对于确定该免疫状态对母亲和胎儿的影响也具有重要价值。这些信息还将为自身免疫性疾病的病因提供进一步线索。

相似文献

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Anti-autologous erythrocyte plaque-forming cells in pregnancy. A parameter of immunoregulatory change.孕期抗自身红细胞斑块形成细胞。免疫调节变化的一个参数。
Vox Sang. 1978;35(5):277-87. doi: 10.1111/j.1423-0410.1978.tb02936.x.
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Fetal human hemolytic plaque-forming cells. Evidence of reactivity to maternal and other erythrocytes.胎儿人类溶血空斑形成细胞。对母体及其他红细胞反应性的证据。
Vox Sang. 1978;35(4):234-40. doi: 10.1111/j.1423-0410.1978.tb02927.x.
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The risk assessment study for hemolytic disease of the fetus and newborn in a University Hospital in Turkey.土耳其一家大学医院中胎儿及新生儿溶血病的风险评估研究。
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Br Med J. 1980 Jun 28;280(6231):1569-71. doi: 10.1136/bmj.280.6231.1569.