PD-1 Regulates T Cell Proliferation in a Tissue and Subset-Specific Manner During Normal Mouse Pregnancy

Shepard, Michelle; Bonney, Elizabeth A.

doi:10.3109/08820139.2013.782317

Cited by 22 publications

(21 citation statements)

References 85 publications

(108 reference statements)

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“…Most research concerning inflammation‐induced preterm labor has therefore focused on the innate limb of immunity . Yet, several studies reported strong evidence that T cells, the primary cellular component of the adaptive immune system, are present at the maternal‐fetal interface . More recently, we provided evidence indicating that T cells are also implicated in the mechanisms that lead to labor at term and spontaneous preterm labor .…”

Section: Introductionmentioning

confidence: 81%

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

Leng

Romero²,

et al. 2019

American J Rep Immunol

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Problem The immunophenotype of B cells at the maternal‐fetal interface (decidua) in labor at term and preterm labor is poorly understood. Method of study Decidual tissues were obtained from women with preterm or term labor and from non‐labor gestational age‐matched controls. Immunophenotyping of decidual B cells was performed using multicolor flow cytometry. Results (a) In the absence of acute or chronic chorioamnionitis, total B cells were more abundant in the decidua parietalis of women who delivered preterm than in those who delivered at term, regardless of the presence of labor; (b) decidual transitional and naïve B cells were the most abundant B‐cell subsets; (c) decidual B1 B cells were increased in women with either labor at term or preterm labor and chronic chorioamnionitis compared to those without this placental lesion; (d) decidual transitional B cells were reduced in women with preterm labor compared to those without labor; (e) naïve, class‐switched, and non–class‐switched B cells in the decidual tissues underwent mild alterations with the process of preterm labor; (f) decidual plasmablasts seemed to increase in women with either labor at term or preterm labor with chronic chorioamnionitis; and (g) decidual B cells expressed high levels of interleukin (IL)‐12, IL‐6, and/or IL‐35. Conclusion Total B cells are not increased with the presence of preterm or term labor; yet, specific subsets (B1 and plasmablasts) undergo alterations in women with chronic chorioamnionitis. Therefore, B cells are solely implicated in the pathological process of preterm labor in a subset of women with chronic inflammation of the placenta. These findings provide insight into the immunology of the maternal‐fetal interface in preterm and term labor.

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Section: Introductionmentioning

confidence: 81%

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

Leng

Romero²,

et al. 2019

American J Rep Immunol

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“…A number of other factors also appear to affect the trafficking of effector T-cells through the decidua, including cytokines (such as TGFβ, IL-10, CCL2), hormones (progesterone, corticotropin-releasing hormone, PGs), Fas-Fas ligand signaling, HLA-G, Programmed Death-1 (PD-1), and other molecules that affect T-cell metabolism (such as tryptophan) (Bonney and Matzinger 1998; Kalantaridou et al 2007; Xiong et al 2010; Silasi and Mor 2012; Shepard and Bonney 2013; Nancy and Erlebacher 2014; Wu et al 2014). Tryptophan is an essential amino required for T-cell activation.…”

Section: Why Does the Human Uterus Only Support A Pregnancy For Nine mentioning

confidence: 99%

Molecular Regulation of Parturition: The Role of the Decidual Clock

Norwitz

Bonney

Snegovskikh

et al. 2015

Cold Spring Harb Perspect Med

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The timing of birth is a critical determinant of perinatal outcome. Despite intensive research, the molecular mechanisms responsible for the onset of labor both at term and preterm remain unclear. It is likely that a “parturition cascade” exists that triggers labor at term, that preterm labor results from mechanisms that either prematurely stimulate or short-circuit this cascade, and that these mechanisms involve the activation of proinflammatory pathways within the uterus. It has long been postulated that the fetoplacental unit is in control of the timing of birth through a “placental clock.” We suggest that it is not a placental clock that regulates the timing of birth, but rather a “decidual clock.” Here, we review the evidence in support of the endometrium/decidua as the organ primarily responsible for the timing of birth and discuss the molecular mechanisms that prime this decidual clock.

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“…[21][22][23][24] We have studied T-cell homeostasis in mice and observed changes in the maternal immune system that persist PP. [21][22][23][25][26][27] There may be accumulation of TREGs in PP that may protect subsequent pregnancies. 28,29 Abnormal pregnancy, including preeclampsia [30][31][32][33][34][35] and preterm birth, 36 is associated with immune system dysregulation.…”

Section: Introductionmentioning

confidence: 99%

Impact of Immune Deficiency on Remodeling of Maternal Resistance Vasculature 4 Weeks Postpartum in Mice

et al. 2017

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Pregnancy manifests changes in the vascular and immune systems that persist postpartum (PP), have important implications for future pregnancies, and may modify responses to cardiovascular stress in late life. The association between immune and vascular function and the generation or progression of cardiovascular disease beg the question of whether altered immunity modifies pregnancy-induced changes in the vasculature. Our objective was to compare changes in the function and remodeling of systemic resistance vessels 4 weeks PP in normal C57BL/6 (B6), and immunodeficient mice recombinase 1-deficient/B6 (Rag1). Immune deficiency did not change the responsiveness to acetylcholine (ACh) and phenylephrine at baseline but decreased arterial distensibility and increased stiffness PP. Adoptive transfer of CD8 T cells into Rag1 À/À mice decreased the response to ACh while increasing distensibility and wall thickness. When compared to PP Rag1 À/À , vessels from PP CD4-deficient mice, which have B cells and CD8 T cells, but no CD4 cells, show increased distensibility and decreased responsiveness to ACh in a pattern similar to that seen in Rag1 À/À given CD8 T cells prior to mating. These studies suggest a key role for T cell, particularly CD8 T cell, associated factors in the PP remodeling of maternal resistance vessels.

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PD-1 Regulates T Cell Proliferation in a Tissue and Subset-Specific Manner During Normal Mouse Pregnancy

Cited by 22 publications

References 85 publications

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

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

Molecular Regulation of Parturition: The Role of the Decidual Clock

Impact of Immune Deficiency on Remodeling of Maternal Resistance Vasculature 4 Weeks Postpartum in Mice

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