scholarly journals Blockade of CD40 ligand for intercellular communication reduces hypertension, placental oxidative stress, and AT1-AA in response to adoptive transfer of CD4+ T lymphocytes from RUPP rats

2015 ◽  
Vol 309 (10) ◽  
pp. R1243-R1250 ◽  
Author(s):  
Denise C. Cornelius ◽  
Javier Castillo ◽  
Justin Porter ◽  
Lorena M. Amaral ◽  
Nathan Campbell ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
T Cells ◽  
T Lymphocytes ◽  
Adoptive Transfer ◽  
Cell Communication ◽  
Cd40 Ligand ◽  
Type I ◽  
Uterine Perfusion ◽  
Placental Ischemia

Preeclampsia (PE) is associated with altered immune activation during pregnancy. We have previously shown that adoptive transfer of CD4+ T cells from the reduced uterine perfusion pressure (RUPP) rat model of PE increases blood pressure, oxidative stress (ROS), and inflammation in normal pregnant recipient rats. The objective of this study was to determine if blockade of communication via the CD40-CD40 ligand (CD40L) interaction between placental ischemia-induced CD4+ T cells with endogenous normal pregnant (NP) cells would improve pathophysiology that was previously observed in NP recipient rats of RUPP CD4+ T cells. Splenic CD4+ T lymphocytes were magnetically separated, incubated with 2.5 μg/ml anti-CD40 ligand (αCD40L) overnight, and transferred into NP rats on day 12 of gestation (NP+RUPP CD4+ T+anti-CD40L). On day 19 of gestation, blood pressure (MAP), blood, and tissues were collected. MAP was 99 ± 2 in NP ( n = 13), 116 ± 4 in NP+RUPP CD4+ T cells ( n = 7; P < 0.01); MAP only increased to 104 ± 2 in NP+RUPP CD4+ T cells+CD40L ( n = 24) ( P < 0.05 vs. NP+RUPP CD4+ T cells). Mechanisms of hypertension in response to RUPP CD4+ T cells include endothelin-1 (ET-1), ROS, and angiotensin II type I receptor (AT1-AA) were analyzed. Inhibition of CD40L binding reduced placental ET-1 to 2.3-fold above NP rats and normalized placental ROS from 318.6 ± 89 in NP+RUPP CD4+ T cells ( P < 0.05) to 118.7 ± 24 in NP+RUPP CD4+ T+anti-CD40L ( P < 0.05). AT1-AA was also normalized with inhibition of CD40L. These data suggest that placental ischemia-induced T-cell communication via the CD40L is one important mechanism leading to much of the pathophysiology of PE.

scholarly journals Activating autoantibodies to the angiotensin II type I receptor play an important role in mediating hypertension in response to adoptive transfer of CD4+ T lymphocytes from placental ischemic rats

2012 ◽  
Vol 302 (10) ◽  
pp. R1197-R1201 ◽  
Author(s):  
Sarah Richards Novotny ◽  
Kedra Wallace ◽  
Judith Heath ◽  
Janae Moseley ◽  
Pushpinder Dhillon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
T Cells ◽  
T Cell ◽  
Angiotensin Ii ◽  
T Lymphocytes ◽  
B Cell ◽  
Inflammatory Cytokines ◽  
Adoptive Transfer ◽  
Type I ◽  
Placental Ischemia

Hypertension in rats with chronic placental ischemia (reduced uterine perfusion pressure, RUPP) is associated with elevated inflammatory cytokines, agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) and CD4+ T cells; all of which are elevated in preclamptic women. Additionally, we have shown that adoptive transfer of RUPP CD4+ T cells increases blood pressure, inflammatory cytokines, and sFlt-1. The objective of this study was to determine the long-term effects of RUPP CD4+ T cells on AT1-AA, renal and systemic hemodynamics in pregnant rats. To answer this question CD4+ T splenocytes were magnetically isolated on day 19 of gestation from control RUPP and normal pregnant (NP) rats and injected into a new group of NP rats at day 13 of gestation. On day 19 of gestation mean arterial pressure (MAP) and renal function (glomerular filtration rates, GFR) were analyzed and serum collected for AT1-AA analysis. To determine a role for AT1-AA to mediate RUPP CD4+ T cell-induced blood pressure increases, MAP was analyzed in a second group of rats treated with AT1 receptor blockade losartan (10 mg·kg−1·day−1) and in a third group of rats treated with rituximab, a B cell-depleting agent (250 mg/kg) we have shown previously to decrease AT1-AA production in RUPP rats. MAP increased from 101 ± 2 mmHg NP to 126 ± 2 mmHg in RUPP rats ( P < 0.001) and to 123 ± 1 mmHg in NP rats injected with RUPP CD4+ T cells (NP+RUPP CD4+T cells) ( P < 0.001). Furthermore, GFR decreased from 2.2 ml/min ( n = 7) in NP rats to 1.0 ml/min ( n = 5) NP+RUPP CD4+T cell. Circulating AT1-AA increased from 0.22 ± 0.1 units in NP rats to 13 ± 0.7 ( P < 0.001) units in NP+RUPP CD4+T cell-treated rats but decreased to 8.34 ± 1 beats/min in NP+RUPP CD4+ T cells chronically treated with rituximab. Hypertension in NP+RUPP CD4+T cell group was attenuated by losartan (102 ± 4 mmHg) and with B cell depletion (101 ± 5 mmHg). Therefore, we conclude that one mechanism of hypertension in response to CD4+ T lymphocytes activated during placental ischemia is via AT1 receptor activation, potentially via AT1-AA during pregnancy.

scholarly journals Hypertension in response to CD4+ T cells from reduced uterine perfusion pregnant rats is associated with activation of the endothelin-1 system

2012 ◽  
Vol 303 (2) ◽  
pp. R144-R149 ◽  
Author(s):  
Kedra Wallace ◽  
Sarah Novotny ◽  
Judith Heath ◽  
Janae Moseley ◽  
James N. Martin ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Adoptive Transfer ◽  
Rat Serum ◽  
Pregnant Rats ◽  
Endothelin 1 ◽  
Induced Hypertension ◽  
Uterine Perfusion ◽  
Placental Ischemia

We have shown that adoptive transfer of CD4+ T cells from placental ischemia (reduction in uteroplacental perfusion, RUPP) rats causes hypertension and elevated inflammatory cytokines during pregnancy. In this study we tested the hypothesis that adoptive transfer of RUPP CD4+ T cells was associated with endothelin-1 activation as a mechanism to increase blood pressure during pregnancy. CD4+ T cells from RUPP or normal pregnant (NP) rats were adoptively transferred into NP rats on gestational day 13. Mean arterial pressure (MAP) was analyzed on gestational day 19, and tissues were collected for endothelin-1 analysis. MAP increased in placental ischemic RUPP rats versus NP rats (124.1 ± 3 vs. 96.2 ± 3 mmHg; P = 0.0001) and increased in NP recipients of RUPP CD4+ T cells (117.8 ± 2 mmHg; P = 0.001 compared with NP). Adoptive transfer of RUPP CD4+ T cells increased placental preproendothelin-1 mRNA 2.1-fold compared with NP CD4+ T cell rats and 1.7-fold compared with NP. Endothelin-1 secretion from endothelial cells exposed to NP rat serum was 52.2 ± 1.9 pg·mg−1·ml−1, 77.5 ± 4.3 pg·mg−1·ml−1 with RUPP rat serum ( P = 0.0003); 47.2 ± .16 pg·mg−1·ml−1 with NP+NP CD4+ T cell serum, and 62.2 ± 2.1 pg·mg−1·ml−1 with NP+RUPP CD4+ T cell serum ( P = 0.002). To test the role of endothelin-1 in RUPP CD4+ T cell-induced hypertension, pregnant rats were treated with an endothelin A (ETA) receptor antagonist (ABT-627, 5 mg/kg) via drinking water. MAP was 92 ± 2 mmHg in NP+ETA blockade and 108 ± 3 mmHg in RUPP+ETA blockade; 95 ± 5 mmHg in NP+NP CD4+ T cells+ETA blockade and 102 ± 2 mmHg in NP+RUPP CD4+ T cells+ETA blockade. These data indicate the importance of endothelin-1 activation to cause hypertension via chronic exposure to activated CD4+ T cells in response to placental ischemia.

scholarly journals Characterization of Mitochondrial Bioenergetics in Preeclampsia

2021 ◽  
Vol 10 (21) ◽  
pp. 5063
Author(s):  
Ramana Vaka ◽  
Evangeline Deer ◽  
Mark Cunningham ◽  
Kristen M. McMaster ◽  
Kedra Wallace ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Cd4 T Cells ◽  
Type I ◽  
Pregnant Rats ◽  
Complex Iv ◽  
Tnf Α ◽  
Placental Ischemia

Preeclampsia (PE) is characterized by new onset hypertension during pregnancy and is associated with oxidative stress, placental ischemia, and autoantibodies to the angiotensin II type I receptor (AT1-AA). Mitochondrial (mt) dysfunction in PE and various sources of oxidative stress, such as monocytes, neutrophils, and CD4 + T cells, have been identified as important players in the pathophysiology of PE. We have established the significance of AT1-AA, TNF-α, and CD4 + T cells in causing mitochondrial (mt) dysfunction in renal and placental tissues in pregnant rats. Although the role of mt dysfunction from freshly isolated intact placental mitochondria has been compared in human PE and normally pregnant (NP) controls, variations among preterm PE or term PE have not been compared and mechanisms contributing to mt ROS during PE are unclear. Therefore, we hypothesized PE placentas would exhibit impaired placental mt function, which would be worse in preterm PE patients than in those of later gestational ages. Immediately after delivery, PE and NP patient’s placentas were collected, mt were isolated and mt respiration and ROS were measured. PE patients at either < or >34 weeks gestational age (GA) exhibited elevated blood pressure and decreased placental mt respiration rates (state 3 and maximal). Patients delivering at >34 weeks exhibited decreased Complex IV activity and expression. Placental mtROS was significantly reduced in both PE groups, compared to NP placental mitochondria. Collectively, the study demonstrates that PE mt dysfunction occurs in the placenta, with mtROS being lower than that seen in NP controls. These data indicate why antioxidants, as a potential target or new therapeutic agent, may not be ideal in treating the oxidative stress associated with PE.

CD4+ T lymphocytes mediate hypercholesterolemia-induced endothelial dysfunction via a NAD(P)H oxidase-dependent mechanism

2008 ◽  
Vol 294 (6) ◽  
pp. H2619-H2626 ◽  
Author(s):  
Ryan M. Wolfort ◽  
Karen Y. Stokes ◽  
D. Neil Granger
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Endothelial Cell ◽  
T Lymphocytes ◽  
Adoptive Transfer ◽  
Cd4 T Cells ◽  
Endothelial Cell Dysfunction ◽  
Superoxide Generation ◽  
Cell Dysfunction ◽  
Ifn Γ

Although hypercholesterolemia is known to impair endothelium-dependent vasodilation (EDV) long before the appearance of atherosclerotic plaques, it remains unclear whether the immune mechanisms that have been implicated in atherogenesis also contribute to the early oxidative stress and endothelial cell dysfunction elicited by hypercholesterolemia. EDV (wire myography), superoxide generation (cytochrome c reduction), and NAD(P)H oxidase mRNA expression were monitored in aortic rings from wild-type (WT) and mutant mice placed on either a normal diet or a cholesterol-enriched diet (HC) for 2 wk. WT mice on HC exhibited impaired EDV, enhanced superoxide generation, and increased expression of NAD(P)H oxidase subunit Nox-2 mRNA. The impaired EDV and increased superoxide generation induced by HC were significantly blunted in severe combined immunodeficient (SCID) mice and CD4+ T lymphocyte-deficient mice. These responses were also attenuated in HC mice genetically deficient in IFN-γ; however, adoptive transfer of WT-HC CD4+ T lymphocytes to IFN-γ-deficient recipients restored HC-induced responses. The HC-induced impaired EDV and oxidative stress were also attenuated in HC mice genetically deficient in Nox-2 (gp91 phox−/−) and in WT→gp91 phox−/−-HC chimeras. HC-induced gp91 phox mRNA expression was significantly blunted in mice deficient in CD4+ T cells or IFN-γ and was restored with adoptive transfer of WT-HC CD4+ T cells to IFN-γ-deficient recipients. These findings implicate the immune system in the early endothelial cell dysfunction associated with hypercholesterolemia and are consistent with a mechanism of impaired EDV that is mediated by CD4+ T cells and IFN-γ, acting through the generation of superoxide from vascular NAD(P)H oxidase.

scholarly journals CD4+ T cells cause renal and placental mitochondrial oxidative stress as mechanisms of hypertension in response to placental ischemia

2021 ◽  
Vol 320 (1) ◽  
pp. F47-F54
Author(s):  
Evangeline Deer ◽  
Kristin E. Reeve ◽  
Lorena Amaral ◽  
Venkata Ramana Vaka ◽  
Michael Franks ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
T Cell ◽  
Mitochondrial Dysfunction ◽  
Nk Cells ◽  
Cd4 T Cells ◽  
Cd4 T Cell ◽  
Mitochondrial Oxidative Stress ◽  
Uterine Perfusion ◽  
Placental Ischemia

The reduced uterine perfusion pressure (RUPP) rat model and normal pregnant (NP) rat recipients of RUPP CD4+ T cells recapitulate many characteristics of preeclampsia such as hypertension and oxidative stress. We have shown an important hypertensive role for natural killer (NK) cells to cause mitochondrial dysfunction in RUPP rats; however, the role for RUPP CD4+ T cells to stimulate NK cells is unknown. Therefore, we hypothesized that RUPP-induced CD4+ T cells activate NK cells to cause mitochondrial dysfunction/reactive oxygen species (ROS) as mechanisms of hypertension during pregnancy. We tested our hypothesis by adoptive transfer of RUPP CD4+ T cells into NP rats or by inhibiting the activation of RUPP CD4+ T cells with Orencia (abatacept) and examining hypertension, NK cells, and mitochondrial function. RUPP was performed on gestation day (GD) 14, and splenic CD4+ T cells were isolated on GD 19 and injected into NP rats on GD 13. In a separate group of rats, Orencia was infused and the RUPP procedure was performed. Mean arterial pressure and placental and renal mitochondrial ROS increased in RUPP ( n = 7, P < 0.05) and NP + RUPP CD4+ T-cell recipients ( n = 13, P < 0.05) compared with control NP ( n = 7) and NP + NP CD4+ T-cell recipients ( n = 5) but was reduced with Orencia ( n = 13, P < 0.05). Placental and renal respiration was reduced in RUPP ( n = 6, P < 0.05) and NP + RUPP CD4+ T-cell recipients ( n = 6, state 3 P < 0.05) compared with NP ( n = 5) and NP + NP CD4+ T-cell recipients ( n = 5) but improved with Orencia ( n = 9, n = 8 P < 0.05). These data indicate that CD4+ T cells, independent of NK cells, cause mitochondrial dysfunction/ROS contributing to hypertension in response to placental ischemia during pregnancy.

scholarly journals An increased population of regulatory T cells improves the pathophysiology of placental ischemia in a rat model of preeclampsia

2015 ◽  
Vol 309 (8) ◽  
pp. R884-R891 ◽  
Author(s):  
Denise C. Cornelius ◽  
Lorena M. Amaral ◽  
Ashlyn Harmon ◽  
Kedra Wallace ◽  
Alexia J. Thomas ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Rat Model ◽  
Perfusion Pressure ◽  
Type I ◽  
Pregnant Rats ◽  
Tnf Α ◽  
Uterine Perfusion ◽  
Placental Ischemia ◽  
One Way Anova

The reduced uterine perfusion pressure (RUPP) rat model of preeclampsia exhibits much of the pathology characterizing this disease, such as hypertension, inflammation, suppressed regulatory T cells (TRegs), reactive oxygen species (ROS), and autoantibodies to the ANG II type I receptor (AT1-AA) during pregnancy. The objective of this study was to determine whether supplementation of normal pregnant (NP) TRegs into RUPP rats would attenuate the pathophysiology associated with preeclampsia during pregnancy. CD4+/CD25+ T cells were isolated from spleens of NP and RUPP rats, cultured, and injected into gestation day (GD) 12 normal pregnant rats that underwent the RUPP procedure on GD 14. On GD 1, mean arterial pressure (MAP) was recorded, and blood and tissues were collected for analysis. One-way ANOVA was used for statistical analysis. MAP increased from 99 ± 2 mmHg in NP ( n = 12) to 127 ± 2 mmHg in RUPP ( n = 21) but decreased to 118 ± 2 mmHg in RUPP+NP TRegs ( n = 17). Circulating IL-6 and IL-10 were not significantly changed, while circulating TNF-α and IL-17 were significantly decreased after supplementation of TRegs. Placental and renal ROS were 339 ± 58.7 and 603 ± 88.1 RLU·min−1·mg−1 in RUPP and significantly decreased to 178 ± 27.8 and 171 ± 55.6 RLU·min−1·mg−1, respectively, in RUPP+NP TRegs; AT1-AA was 17.81 ± 1.1 beats per minute (bpm) in RUPP but was attenuated to 0.50 ± 0.3 bpm with NP TRegs. This study demonstrates that NP TRegs can significantly improve inflammatory mediators, such as IL-17, TNF-α, and AT1-AA, which have been shown to increase blood pressure during pregnancy.

scholarly journals CD40/CD40L contributes to hypercholesterolemia-induced microvascular inflammation

2009 ◽  
Vol 296 (3) ◽  
pp. H689-H697 ◽  
Author(s):  
Karen Y. Stokes ◽  
LeShanna Calahan ◽  
Candiss M. Hamric ◽  
Janice M. Russell ◽  
D. Neil Granger
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
T Cell ◽  
Blood Cell ◽  
Cell Function ◽  
Inflammatory Responses ◽  
Microvascular Dysfunction ◽  
Cd40 Ligand ◽  
Scid Mice ◽  
Endothelial Cell Function

Hypercholesterolemia is associated with phenotypic changes in endothelial cell function that lead to a proinflammatory and prothrombogenic state in different segments of the microvasculature. CD40 ligand (CD40L) and its receptor CD40 are ubiquitously expressed and mediate inflammatory responses and platelet activation. The objective of this study was to determine whether CD40/CD40L, in particular T-cell CD40L, contributes to microvascular dysfunction induced by hypercholesterolemia. Intravital microscopy was used to quantify blood cell adhesion in cremasteric postcapillary venules, endothelium-dependent vasodilation responses in arterioles, and microvascular oxidative stress in wild-type (WT) C57BL/6, CD40-deficient (−/−), CD40L−/−, or severe combined immune deficient (SCID) mice placed on a normal (ND) or high-cholesterol (HC) diet for 2 wk. WT-HC mice exhibited an exaggerated leukocyte and platelet recruitment in venules and impaired vasodilation responses in arterioles compared with ND counterparts. A deficiency of CD40, CD40L, or lymphocytes attenuated these responses to HC. The HC phenotype was rescued in CD40L−/− and SCID mice by a transfer of WT T cells. Bone marrow chimeras revealed roles for both vascular- and blood cell-derived CD40 and CD40L in the HC-induced vascular responses. Hypercholesterolemia induced an oxidative stress in both arterioles and venules of WT mice, which was abrogated by either CD40 or CD40L deficiency. The transfer of WT T cells into CD40L−/− mice restored the oxidative stress. These results implicate CD40/CD40L interactions between circulating cells and the vascular wall in both the arteriolar and venular dysfunction elicited by hypercholesterolemia and identify T-cell-associated CD40L as a key mediator of these responses.

CD40 LIGAND MUTATIONS IN X-LINKED IMMUNODEFICIENCY WITH HYPER-IgM

PEDIATRICS ◽  
1994 ◽  
Vol 94 (2) ◽  
pp. 280-280
Author(s):  
Arden Levy ◽  
Andrew Liu
Keyword(s):  
T Cells ◽  
B Cells ◽  
Bacterial Infections ◽  
Point Mutations ◽  
Cell Communication ◽  
Cd40 Ligand ◽  
Research Groups ◽  
Immune Disorder ◽  
Hyper Igm

Purpose of the Studies. Hyper-IgM immunodeficiency is characterized by recurrent bacterial infections, normal or elevated IgM, and markedly decreased IgG, IgA, and IgE. Previous research suggested that the T cells of these patients are defective in their ability to help B cells make functional antibody. CD40 ligand (CD4OL) is a membrane glycoprotein on activated T helper cells and binds the CD40 molecule expressed on B cells, and induces proliferation and immunoglobulin class switching (in conjunction with IL-4). The gene for the CD4OL has been mapped to position q26.3-q27.1 on chromosome X (same as the Hyper-IgM gene and the area of isotype switching). Several research groups sought to determine if the immunodeficiency in Hyper-IgM patients is due to defective CD4OL. Findings. The five papers listed above document the work of different research groups that simultaneously found abnormalities in the CD4OL gene in a total of 16 patients with X-linked Hyper-IgM syndrome. Different mutations of the CD4OL gene have been discovered, including point mutations, deletions, and nonsense sequences. Mutant version of CD4OL taken from Hyper IgM patients were unable to "help" B cells in vitro. Thus, deficient CD40/CD40L interactions between B and T cells results in severely impaired immunity. Restricted CD40L gene expression to T cells may ultimately allow gene therapy as treatment. Reviewers' Comments. A concise editorial by Jean Marx entitled "Cell Communication Failure Leads to Immune Disorder" describes this landmark research and accompanies the Spriggs article in the February 12th issue of Science (pp. 896-897). This discovery may not only lead to treatment of this disorder, but also modification of other less favorable immune responses.

Splenocyte transfer from hypertensive donors eliminates premenopausal female protection from Ang II-induced hypertension

2022 ◽  
Author(s):  
Megan A Sylvester ◽  
Dennis P Pollow ◽  
Caitlin Moffett ◽  
Wendy Nunez ◽  
Jennifer L Uhrlaub ◽  
...  
Keyword(s):  
Blood Pressure ◽  
T Cells ◽  
Adoptive Transfer ◽  
T Regulatory Cells ◽  
Estrogen Signaling ◽  
Ang Ii ◽  
Regulatory Cells ◽  
Adaptive Immune Cells ◽  
Induced Hypertension ◽  
Rag 1

Premenopausal females are protected from Angiotensin II (Ang II)-induced hypertension following the adoptive transfer of T cells from normotensive donors. For the present study, we hypothesized that the transfer of hypertensive T cells (HT) or splenocytes (HS) from hypertensive donors would eliminate premenopausal protection from hypertension. Premenopausal Rag-1-/- females received either normotensive (NT) or hypertensive cells, three weeks prior to Ang II infusion (14 days, 490 ng/kg/min). Contrary to our hypothesis, no increase in Ang II-induced blood pressure was observed in the NT/Ang or HT/Ang groups. Flow cytometry demonstrated that renal FoxP3+ T regulatory cells were significantly decreased and IHC showed an increase in renal F4/80+ macrophages in HT/Ang, suggesting a shift in the renal inflammatory environment despite no change in blood pressure. Renal mRNA expression of MCP-1, Endothelin-1, GPER-1 were significantly decreased in HT/Ang. The adoptive transfer of hypertensive splenocytes prior to Ang II infusion (HS/Ang) eliminated premenopausal protection from hypertension and significantly decreased splenic FoxP3+ T regulatory cells compared to females receiving normotensive splenocytes (NS/Ang). Expression of MIP-1a/CCL3, a potent macrophage chemokine was elevated in HS/Ang, however no increase in renal macrophage infiltration occurred. Together, these data show that in premenopausal females T cells from hypertensive donors are not sufficient to induce a robust Ang II mediated hypertension, in contrast, transfer of hypertensive splenocytes (consisting of T/B lymphocytes, dendritic cells, macrophages) is sufficient. Further work is needed to understand how innate and adaptive immune cells and estrogen signaling coordinate to cause differential hypertensive outcomes in premenopausal females.

scholarly journals Oxidative stress signaling in response to CD 4+ T cells stimulated via placental ischemia play an important role in hypertension during preeclampsia (860.14)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Jeremy Scott ◽  
Kedra Wallace ◽  
Denise Cornelius ◽  
Lorena Amaral ◽  
Janae Moseley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Stress Signaling ◽  
Placental Ischemia
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