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Proliferation of endogenous regulatory T cells improve the pathophysiology associated with placental ischaemia of pregnancy
Author(s) -
Ibrahim Tarek,
Przybyl Lukasz,
Harmon Ashlyn C.,
Amaral Lorena M.,
Faulkner Jessica L.,
Cornelius Denise C.,
Cunningham Mark W.,
Hünig Thomas,
Herse Florian,
Wallukat Gerd,
Dechend Ralf,
LaMarca Babbette
Publication year - 2017
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12724
Subject(s) - preeclampsia , medicine , endocrinology , endogeny , pathophysiology , blood pressure , inflammation , fetus , pregnancy , biology , genetics
Problem Preeclampsia (PE) is associated with inflammation and decreased Treg cells and IL‐10. The reduced uterine perfusion pressure (RUPP) rat model of PE exhibits these characteristics, and we hypothesized that induction of endogenous Tregs by a specific stimulus (CD28 superagonistic monoclonal antibody) would reduce inflammation, vasoactive factors, and hypertension in RUPP rats. Method of study RUPP was performed at gestation day (GD) 14; CD28 superagonist was administered intraperitoneally GD15; GD18 carotid catheters were inserted, and GD19 MAP and pup weight, blood, and tissues were collected. Results MAP (mmHg) in NP rats was 99±5 and 122±2 in RUPPs and was 111±1 mmHg in RUPP+SA. Circulating Tregs were 6±2% in NP rats and 0.77±0.49% in RUPP rats but increased to 11± 3% in RUPP+SA rats. Circulating IL‐6 and IL‐2 were decreased while IL‐10 and TGF‐B were significantly increased in RUPP+SA compared to RUPP controls. Vasoactive pathways such as ET‐1, AT1‐AA, and ROS were all reduced in RUPP+SA compared to RUPP. Pup weight was 2.4±0.05 mg in NP and 1.94±0.062 mg in RUPP and increased to 2.1± 0.05 mg in RUPP+SA. Conclusion These data suggest that stimulating endogenous Tregs lower factors causing hypertension and can improve fetal weight in response to PE.