Regulatory B Cells in Pregnancy: Lessons from Autoimmunity, Graft Tolerance, and Cancer.

Regulatory B Cells in Pregnancy: Lessons from Autoimmunity, Graft Tolerance, and Cancer.
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DOI:
10.3389/fimmu.2017.00172
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发表时间:
2017
影响因子:
7.3
通讯作者:
Diener KR
Diener KR
中科院分区:
医学2区
文献类型:
--
作者:
Guzman-Genuino RM;Diener KR

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怀孕的成功取决于母体免疫系统识别和适应正在生长的半同种异体胎儿。能够进行负调节的特殊淋巴细胞亚群是这一过程的基础,其中包括调节性 T 细胞 (Treg) 和潜在的调节性 B 细胞 (Breg)。我们目前对 Bregs 免疫调节作用的理解大部分来自自身免疫、移植耐受和癌症生物学领域的研究。 Bregs 控制自身免疫性疾病,并可以通过抑制效应 T 细胞和树突状细胞 (DC) 的分化以及激活 Tregs 来引发移植物耐受。此外,在癌症中,Bregs 被肿瘤细胞劫持以促进肿瘤发生。因此,怀孕代表了协调这些领域的条件——必须建立机制来确保母体在整个怀孕期间的免疫耐受性,以允许半同种异体胎儿在其中生长。因此,Breg 在自身免疫性疾病、移植耐受和癌症中的作用机制也可能发生在妊娠期间。在这篇综述中,我们讨论了 Breg 作为妊娠守护者的潜在作用,并提出了一种内分泌调节反馈回路,强调了 Breg-Treg-致耐受性 DC 界面对于诱导母体免疫耐受至关重要。
The success of pregnancy is contingent on the maternal immune system recognizing and accommodating a growing semi-allogeneic fetus. Specialized subsets of lymphocytes capable of negative regulation are fundamental in this process, and include the regulatory T cells (Tregs) and potentially, regulatory B cells (Bregs). Most of our current understanding of the immune regulatory role of Bregs comes from studies in the fields of autoimmunity, transplantation tolerance, and cancer biology. Bregs control autoimmune diseases and can elicit graft tolerance by inhibiting the differentiation of effector T cells and dendritic cells (DCs), and activating Tregs. Furthermore, in cancer, Bregs are hijacked by neoplastic cells to promote tumorigenesis. Pregnancy therefore represents a condition that reconciles these fields—mechanisms must be in place to ensure maternal immunological tolerance throughout gravidity to allow the semi-allogeneic fetus to grow within. Thus, the mechanisms underlying Breg activities in autoimmune diseases, transplantation tolerance, and cancer may take place during pregnancy as well. In this review, we discuss the potential role of Bregs as guardians of pregnancy and propose an endocrine-modulated feedback loop highlighting the Breg–Treg–tolerogenic DC interface essential for the induction of maternal immune tolerance.