Long-term fetal microchimerism in peripheral blood mononuclear cell subsets in healthy women and women with scleroderma
Long-term fetal microchimerism in peripheral blood mononuclear cell subsets in healthy women and women with scleroderma
复制标题
DOI：
10.1182/blood.v93.6.2033.406k18_2033_2037
复制
发表时间：
1999-03-15
期刊：
影响因子：
20.3
通讯作者：
Nelson, JL
中科院分区：
文献类型：
--
作者：
Evans, PC;Lambert, N;Nelson, JL
最近发现胎儿CD34(+) CD38(+)细胞在妊娠后多年仍存留在母体外周血中。 CD34(+) CD38(+)细胞是祖细胞，可以分化为成熟的免疫活性细胞。我们询问既往妊娠妇女的 T 淋巴细胞、B 淋巴细胞、单核细胞和自然杀伤细胞群是否存在长期胎儿微嵌合现象。我们以有儿子的女性为目标，使用聚合酶链反应检测 Y 染色体特异性序列，以测试从外周血单核细胞 (PBMC) 以及 CD3、CD19、CD14 和 CD56/16 排序子集中提取的 DNA。我们还询问持续的微嵌合现象是否可能导致母亲随后患上自身免疫性疾病，其中包括患有自身免疫性疾病硬皮病的女性。硬皮病在育龄后的女性中发病率最高，其临床与异基因造血干细胞移植后发生的慢性移植物抗宿主病相似。已知涉及嵌合现象。对 68 名经产女性的 PBMC 中的男性 DNA 进行了研究，对 20 名经产女性的 PBMC 子集进行了研究。在 33%（48 名中的 16 名）健康女性和 60%（20 名中的 12 名）患有硬皮病的女性的 PBMC 中发现微嵌合，P = 0.046。在一些女性的CD3、CD19中发现了微嵌合体。 CD14。 CD56/16 亚群包括妊娠后 38 岁以内。硬皮病患者的 PBMC 亚群中的微嵌合现象并不比健康对照者明显更频繁。总体而言，大约三分之一的女性在 CD3、CD19 和 CD14 亚群中发现了微嵌合体，在一半的女性中发现了 CD56/16 亚群中存在微嵌合体。母亲和儿子的 HLA 分型表明，HLA 相容性并不是 PBMC 亚群中持续微嵌合的必要条件。面对 HLA 差异，胎儿微嵌合现象意味着存在特定的母体免疫调节途径，允许这些细胞在正常女性中持续存在，但阻止其效应功能。尽管 PBMC 中的微嵌合现象在患有硬皮病的女性中比健康对照更常见，但仍需要进行额外的研究来确定微嵌合现象是否在这种或其他自身免疫性疾病的发病机制中发挥作用。 (C) 1999 年，美国血液学会。
Fetal CD34(+) CD38(+) cells have recently been found to persist in maternal peripheral blood for many years after pregnancy. CD34(+) CD38(+) cells are progenitor cells that can differentiate into mature immune-competent cells. We asked whether long-term fetal microchimerism occurs in T lymphocyte, B lymphocyte, monocyte, and natural-killer cell populations of previously pregnant women. We targeted women with sons and used polymerase chain reaction for a Y-chromosome-specific sequence to test DNA extracted from peripheral blood mononuclear cells (PBMC) and from CD3, CD19, CD14, and CD56/16 sorted subsets. We also asked whether persistent microchimerism might contribute to subsequent autoimmune disease in the mother and included women with the autoimmune disease scleroderma. Scleroderma has a peak incidence in women after childbearing years and has clinical similarities to chronic graft-versus-host disease that occurs after allogeneic hematopoietic stem-cell transplantation. known to involve chimerism. Sixty-eight parous women were studied for male DNA in PBMC and 20 for PBMC subsets. Microchimerism was found in PBMC from 33% (16 of 48) of healthy women and 60% (12 of 20) women with scleroderma, P = .046. Microchimerism was found in some women in CD3, CD19. CD14. and CD56/16 subsets including up to 38 years after pregnancy. Microchimerism in PBMC subsets was not appreciably more frequent in scleroderma patients than in healthy controls. Overall, microchimerism was found in CD3, CD19, and CD14 subsets in approximately one third of women and in CD56/16 in one half of women. HLA typing of mothers and sons indicated that HLA compatibility was not a requirement for persistent microchimerism in PBMC subsets. Fetal microchimerism in the face of HLA disparity implies that specific maternal immunoregulatory pathways exist that permit persistence but prevent effector function of these cells in normal women. Although microchimerism in PBMC was more frequent in women with scleroderma than healthy controls additional studies will be necessary to determine whether microchimerism plays a role in the pathogenesis of this or other autoimmune diseases. (C) 1999 by The American Society of Hematology.