An imbalance between innate and adaptive immune cells at the maternal–fetal interface occurs prior to endotoxin-induced preterm birth

Arenas‐Hernandez, Marcia; Romero, Roberto; Louis, D St.; Hassan, Sonia S.; Kaye, Emily B; Gomez‐Lopez, Nardhy

doi:10.1038/cmi.2015.22

Cited by 68 publications

(75 citation statements)

References 77 publications

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“…In addition, maternal CD8+ regulatory T cells have been implicated in the systemic and local (i.e. the maternal-fetal interface) immune mechanisms that lead to spontaneous preterm labor [70, 71]. CD8+ regulatory T cells are induced extrathymically through antigen presentation in the neonatal period in mice [72]; however, their role in humans is unknown.…”

Section: Discussionmentioning

confidence: 99%

CD71+ erythroid cells from neonates born to women with preterm labor regulate cytokine and cellular responses

Miller

Romero

Unkel

et al. 2018

Journal of Leukocyte Biology

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Neonatal CD71+ erythroid cells are thought to have immunosuppressive functions. Recently, we demonstrated that CD71+ erythroid cells from neonates born to women who underwent spontaneous preterm labor are reduced to levels similar to those of term neonates; yet, their functional properties are unknown. Herein, we investigated the functionality of CD71+ erythroid cells from neonates born to women who underwent spontaneous preterm or term labor. CD71+ erythroid cells from neonates born to women who underwent spontaneous preterm labor displayed a similar mRNA profile to that of those from term neonates. The direct contact between preterm or term neonatal CD71+ erythroid cells and maternal mononuclear immune cells, but not soluble products from these cells, induced the release of pro-inflammatory cytokines and a reduction in the release of TGFβ. Moreover, PTL-derived neonatal CD71+ erythroid cells: 1) modestly altered CD8+ T cell activation; 2) inhibited conventional CD4+ and CD8+ T-cell expansion; 3) suppressed the expansion of CD8+ regulatory T cells,; 4) regulated cytokine responses mounted by myeloid cells in the presence of a microbial product; and 5) indirectly modulated T-cell cytokine responses. In conclusion, neonatal CD71+ erythroid cells regulate neonatal T-cell and myeloid responses and their direct contact with maternal mononuclear cells induces a pro-inflammatory response. These findings provide insight into the biology of neonatal CD71+ erythroid cells during the physiologic and pathologic processes of labor.

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Section: Discussionmentioning

confidence: 99%

CD71+ erythroid cells from neonates born to women with preterm labor regulate cytokine and cellular responses

Miller

Romero

Unkel

et al. 2018

Journal of Leukocyte Biology

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“…CD changes are of particular interest in PTL, where it has been shown that CD56+ NK cells and T cells are increased (Hamilton et al 2013) along with an elevated expression of CCL8, which is a chemoattractant for NK and T cells (Proost et al 1996). These inflammatory changes implicate both the innate and adaptive immune system in the pathological process of PTL and interestingly the imbalance among these two immune systems in PTL have been demonstrated via a mouse model (Arenas-Hernandez et al 2016).…”

Section: Choriodecidua (Cd)mentioning

confidence: 99%

“…The aetiology of sterile intra-amniotic inflammation is unknown; however, the inflammation is understood to result from activation of the innate immune system by endogenous danger signals, derived from necrosis or cellular stress, termed damage-associated molecular pattern molecules, or alarmins (Gomez-Lopez et al 2016). One such alarmin is HMGB1, which has been shown to induce PTL in a mouse model (Gomez-Lopez et al 2016). For further detail on proposed theories on sterile inflammation please refer to Faranak Behnia's review (Behnia et al 2016).…”

Section: Figurementioning

confidence: 99%

Myometrial cytokines and their role in the onset of labour

Sivarajasingam

Imami

Johnson

2016

Journal of Endocrinology

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Human labour is an inflammatory event, physiologically driven by an interaction between hormonal and mechanical factors and pathologically associated with infection, bleeding and excessive uterine stretch. The initiation and communicators of inflammation is still not completely understood; however, a key role for cytokines has been implicated. We summarise the current understanding of the nature and role of cytokines, chemokines and hormones and their involvement in signalling within the myometrium particularly during labour.

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“…Fetal antigen-specific Tregs (regulatory T cells) maintain maternal-fetal tolerance throughout pregnancy [3,4,124]. In contrast, effector T cells infiltrate into the maternal-fetal interface and are implicated in the processes of term [65,[125][126][127] and preterm [17,25,[128][129][130] parturition.…”

Section: A Role For T Cells In Pregnancymentioning

confidence: 99%

“…A breakdown of maternal-fetal tolerance has been implicated in the mechanisms of disease responsible for a subset of recurrent pregnancy loss [10], fetal death [11,12], preterm labor [13][14][15][16][17][18], preterm prelabor rupture of the membranes (preterm PROM) [15] and other obstetrical complications [19][20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Chronic inflammatory lesions of the placenta are associated with an up-regulation of amniotic fluid CXCR3: A marker of allograft rejection

Maymon

Romero

Bhatti

et al. 2018

Journal of Perinatal Medicine

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Objective: The objective of this study is to determine whether the amniotic fluid (AF) concentration of soluble CXCR3 and its ligands CXCL9 and CXCL10 changes in patients whose placentas show evidence of chronic chorioamnionitis or other placental lesions consistent with maternal anti-fetal rejection. Methods: This retrospective case-control study included 425 women with (1) preterm delivery (n = 92); (2) term in labor (n = 68); and (3) term not in labor (n = 265). Amniotic fluid CXCR3, CXCL9 and CXCL10 concentrations were determined by ELISA. Results: (1) Amniotic fluid concentrations of CXCR3 and its ligands CXCL9 and CXCL10 are higher in patients with preterm labor and maternal anti-fetal rejection lesions than in those without these lesions [CXCR3: preterm labor and delivery with maternal anti-fetal rejection placental lesions (median, 17.24 ng/mL; IQR, 6.79-26.68) vs. preterm labor and delivery without these placental lesions (median 8.79 ng/mL; IQR, 4.98-14.7; P = 0.028)]; (2) patients with preterm labor and chronic chorioamnionitis had higher AF concentrations of CXCL9 and CXCL10, but not CXCR3, than those without this lesion [CXCR3: preterm labor with chronic chorioamnionitis (median, 17.02 ng/mL; IQR, 5.57-26.68) vs. preterm labor without chronic chorioamnionitis (median, 10.37 ng/mL; IQR 5.01-17.81; P = 0.283)]; (3) patients with preterm labor had a significantly higher AF concentration of CXCR3 than those in labor at term regardless of the presence or absence of placental lesions. Conclusion: Our findings support a role for maternal antifetal rejection in a subset of patients with preterm labor.

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An imbalance between innate and adaptive immune cells at the maternal–fetal interface occurs prior to endotoxin-induced preterm birth

Cited by 68 publications

References 77 publications

CD71+ erythroid cells from neonates born to women with preterm labor regulate cytokine and cellular responses

CD71+ erythroid cells from neonates born to women with preterm labor regulate cytokine and cellular responses

Myometrial cytokines and their role in the onset of labour

Chronic inflammatory lesions of the placenta are associated with an up-regulation of amniotic fluid CXCR3: A marker of allograft rejection

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