ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2015
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.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Analysis of the evolution of placental oxidative stress research from a bibliometric perspective.Frontiers in pharmacology · 2024Pooled it
- Immune Cells in Preeclampsia.International journal of molecular sciences · 2025Review
- Preeclamptic Placental CD19+ B Cells Are Causal to Hypertension During Pregnancy.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Article
- The role of T cell stimulated agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) in mediating multiorgan dysfunction in IL-17 induced hypertension during pregnancy.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024Article
- AT1-AA Is Produced in Offspring in Response to Placental Ischemia and Is Lowered by B-Cell Depletion Without Compromising Overall Offspring Health.Journal of the American Heart Association · 2024Article
- Inhibiting B cell activating factor attenuates preeclamptic symptoms in placental ischemic rats.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- The role of immune cells and mediators in preeclampsia.Nature reviews. Nephrology · 2023Review
- B2 cells contribute to hypertension and natural killer cell activation possibly via AT1-AA in response to placental ischemia.American journal of physiology. Renal physiology · 2023Article
- Setting a stage: Inflammation during preeclampsia and postpartum.Frontiers in physiology · 2023Review
- Review
- Cellular immune responses in the pathophysiology of preeclampsia.Journal of leukocyte biology · 2022Review
- Placental CD4Exploration of medicine · 2022Article
- Therapeutic targeting of inflammation in hypertension: from novel mechanisms to translational perspective.Cardiovascular research · 2021Review
- Investigation of interleukin-2-mediated changes in blood pressure, fetal growth restriction, and innate immune activation in normal pregnant rats and in a preclinical rat model of preeclampsia.Biology of sex differences · 2021Article
- Splenocyte transfer exacerbates salt-sensitive hypertension in rats.Experimental physiology · 2020Article
- Hypertension: a new treatment for an old disease? Targeting the immune system.British journal of pharmacology · 2019Review
- Inflammatory mediators: a causal link to hypertension during preeclampsia.British journal of pharmacology · 2019Review
- Identifying immune mechanisms mediating the hypertension during preeclampsia.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Review
- Vitamin D supplementation improves pathophysiology in a rat model of preeclampsia.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
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Authors and funding
14 authors at 4 institutions in 2 countries.
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Abstract
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.
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