Are B cells altered in the decidua of women with preterm or term labor?

Leng, Yaozhu; Romero, Roberto; Xu, Yi; Galaz, José; Slutsky, Rebecca; Arenas‐Hernandez, Marcia; Garcia‐Flores, Valeria; Motomura, Kenichiro; Hassan, Sonia S.; Reboldi, Andrea; Gomez‐Lopez, Nardhy

doi:10.1111/aji.13102

Cited by 27 publications

(21 citation statements)

References 202 publications

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“…These results are consistent with our results of a ∼1.5fold increase in CD19 + CD20 + B cells numbers in the decidua parietalis in Rhesus macaque exposed to intraamniotic LPS compared to IA saline controls (84). Functionally, B cells were reported to be protective for preterm birth in mice via IL-33 and progesterone-induced blocking factor, decreasing LPS induced neutrophil recruitment (139), although this protective action has been questioned in a recent study (138).…”

Section: B Cellssupporting

confidence: 91%

“…Furthermore, B cell frequency did not significantly change during the course of pregnancy in decidua basalis even during systemic inflammation (231). However, the frequency of CD19 + B cells were higher in the decidua parietalis of women who underwent preterm birth regardless of labor (138,139). These results are consistent with our results of a ∼1.5fold increase in CD19 + CD20 + B cells numbers in the decidua parietalis in Rhesus macaque exposed to intraamniotic LPS compared to IA saline controls (84).…”

Section: B Cellssupporting

confidence: 89%

“…Although B-cell deficient mice have normal pregnancies, IL10 producing B cells protected fetuses from intrauterine demise when exposed to LPS (140). In human term and preterm pregnancy, total CD19 + B cells represent a small fraction (<5%) of decidual leukocytes in both the decidua parietalis and basalis (138,231). Furthermore, B cell frequency did not significantly change during the course of pregnancy in decidua basalis even during systemic inflammation (231).…”

Section: B Cellsmentioning

confidence: 98%

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Immunobiology of Acute Chorioamnionitis

2020

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Acute chorioamnionitis is characterized by neutrophilic infiltration and inflammation at the maternal fetal interface. It is a relatively common complication of pregnancy and can have devastating consequences including preterm labor, maternal infections, fetal infection/inflammation, fetal lung, brain, and gastrointestinal tract injury. In this review, we will discuss current understanding of the pathogenesis, immunobiology, and mechanisms of this condition. Most commonly, acute chorioamnionitis is a result of ascending infection with relatively low-virulence organisms such as the Ureaplasma species. Furthermore, recent vaginal microbiome studies suggest that there is a link between vaginal dysbiosis, vaginal inflammation, and ascending infection. Although less common, microorganisms invading the maternal-fetal interface via hematogenous route (e.g., Zika virus, Cytomegalovirus, and Listeria) can cause placental villitis and severe fetal inflammation and injury. We will provide an overview of the knowledge gleaned from different animal models of acute chorioamnionitis and the role of different immune cells in different maternal-fetal compartments. Lastly, we will discuss how infectious agents can break the maternal tolerance of fetal allograft during pregnancy and highlight the novel future therapeutic approaches.

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Section: B Cellssupporting

confidence: 91%

Section: B Cellssupporting

confidence: 89%

Section: B Cellsmentioning

confidence: 98%

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Immunobiology of Acute Chorioamnionitis

2020

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“…In addition, IL‐35 was tested in the decidua of women after delivery. These studies showed for the first time that the frequency of B cells (CD45 + CD3 ‐ CD19 + CD20 + ) expressing IL‐35 was higher than the percentage of these cells expressing other cytokines (IFN‐γ, IL‐2, IL‐4, IL‐6, IL‐10, IL‐12, TNF‐α) in the decidua basalis …”

Section: Resultsmentioning

confidence: 93%

Regulatory B cells with IL‐35 and IL‐10 expression in a normal and abortion‐prone murine pregnancy model

Sławek

Lorek

Kędzierska

et al. 2019

American J Rep Immunol

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Determination of appropriate immunological interactions between the mother and the fetus and the establishment of immune tolerance are fundamental prerequisites for a successful pregnancy. Among them, the induction of a tolerogenic response to paternal antigens is considered necessary for the success of pregnancy. Disturbed immune tolerance can cause pregnancy disorders, such as spontaneous and recurrent miscarriages or preeclampsia. The crucial work of Aluvihare et al published in 2004 1 indicated for the first time that cell population with the CD4 + CD25 + phenotype played a leading role in maintaining pregnancy in mice. Following studies unambiguously confirmed that these were Treg cells characterized by the CD4 + CD25 + Foxp3 + phenotype. 2,3 It has been proven that in humans, there is an increase in Treg number during normal pregnancy and a decrease in their number and activity in spontaneous abortion cases. 3 It was also confirmed in the murine abortion-prone model of pregnancy (characterized by high rate of fetal resorption and Abstract Problem: Interleukin 35 is a relatively newly discovered cytokine that is produced by regulatory B cells (Bregs) and contributes to their suppressive function, which may contribute to fetal tolerance development and pregnancy maintenance. Therefore, the aim of this study was to determine the frequency of Bregs and expression of IL-35 and IL-10 in these cells in a normal and abortion-prone murine pregnancy model. Methods of study:The frequency of Bregs and expression level of IL-35 and IL-10 in these cells were measured in peripheral blood, uterine draining lymph nodes, uterus, and decidua using flow cytometry. The analysis was performed on days 3 and 14 of pregnancy in normal mice (CBA/JxBALB/c) and abortion-prone (CBA/JxDBA/2J) murine pregnancy model. Results: A decreased percentage of Breg cells expressing IL-35 on day 3 of pregnancyin the uterine draining lymph nodes and in peripheral blood in mice from the abortion group compared with the normal pregnancy group was observed. A similar decrease was also observed in the Breg cells population producing IL-10 in peripheral blood. In the uterus (3 dpc) and decidua (14 dpc), a lower percentage of CD19 + IL-35 + was also noted in the abortion-prone model. Conclusion:We indicated that the early stages of abortion-prone pregnancy (3 dpc) in mice were characterized by diminished frequency of B cells producing IL-35 at both local and peripheral levels. These results and the observed lower level of IL-35 in women suffering from recurrent spontaneous abortion suggest that IL-35 may be involved in the maintenance of pregnancy. K E Y W O R D Sabortion-prone, interleukin 35, maintenance of pregnancy, regulatory B cells

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“…Our laboratory and others have extensively demonstrated that the B cell compartment undergoes significant adaptations during pregnancy, apparently to support the acceptance of the semiallogeneic fetus (12)(13)(14)(15)(16)(17)(18)(19) and to avoid the occurrence of immune mediated pregnancy disorders, like preterm birth (PTB) among others (15,(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). Moreover, it has recently been demonstrated that decidual B cells, through a mechanism involving IL-33, can control inflammation induced by bacterial components and significantly reduce the occurrence of PTB (31).…”

Section: Introductionmentioning

confidence: 99%

Expression of IL-33 Receptor Is Significantly Up-Regulated in B Cells During Pregnancy and in the Acute Phase of Preterm Birth in Mice

et al. 2020

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Interleukin-33 (IL-33) is a mucosal alarmin belonging to the IL-1 cytokine family and is now recognized to have a key role in innate and adaptive immunity, contributing to tissue homeostasis and response to environmental stresses. In addition, IL-33 has also been shown to work as a positive regulator that initiates and maintains a Th2 immune response. In the context of pregnancy, it has been recently demonstrated that upon certain stress conditions, such as an infection induced inflammation, IL-33 is released from the uterine mucosa and triggers decidual B cells to produce anti-inflammatory molecules, which in turn restore immune homeostasis and prevents the development of preterm birth. In this study we therefore performed a detailed characterization of IL-33 receptor (Il1rl1 or ST2) expression in B cells during normal pregnancy, as well as in a mouse model of preterm birth. We observed that splenic B cells significantly up-regulate the expression of Il1rl1 during pregnancy and identified the B1 B cell population as the main ST2-expressing B cell subset. A further kinetic analysis showed that percentages of ST2-expressing B1 B cells are significantly augmented on days 12 and 14 of pregnancy, both in the spleen and peritoneal cavity of pregnant mice, and then drop toward the end of pregnancy to the levels observed in non-pregnant animals. Furthermore, using a mouse model of LPS-induced preterm birth, we demonstrated that not only are the percentages of ST2-expressing B1 B cells significantly enlarged in the spleen during the acute phase of preterm birth, but decidual B cells also significantly up-regulate ST2 expression as compared to term-pregnant mice. Overall, our results suggest a functional role of ST2 expression in B cells during pregnancy and reinforce the importance of the IL-33/ST2 axis in B cells as a critical mechanism to control inflammation-induced preterm birth.

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Are B cells altered in the decidua of women with preterm or term labor?

Cited by 27 publications

References 202 publications

Immunobiology of Acute Chorioamnionitis

Immunobiology of Acute Chorioamnionitis

Regulatory B cells with IL‐35 and IL‐10 expression in a normal and abortion‐prone murine pregnancy model

Expression of IL-33 Receptor Is Significantly Up-Regulated in B Cells During Pregnancy and in the Acute Phase of Preterm Birth in Mice

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