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IL\u201017 can serve as a signal for either the adaptive or innate immune activation. We have previously shown that IL\u201017 contributes to increased blood pressure in association with elevated TH17 cells, NK cells and B cells secreting angiotensin II type 1 receptor agonistic autoantibodies (AT1\u2010AA) during pregnancy. Moreover, we have shown an important role for CD4+T cells and AT1\u2010AA in multiorgan dysfunction as measured by mitochondrial oxidative stress (mt ROS). However, we do not know the role of adaptive immune cells such as T cells or B cells secreting AT1\u2010AA in mediating the PE phenotype in response to elevated IL\u201017.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method of study<\/jats:title>\n                    <jats:p>In order to answer this question, we infused IL\u201017 (150 pg\/day i.p.) into either Sprague Dawley (SD) or athymic nude rats via mini\u2010osmotic pump from gestational day (GD) 14\u201319 of pregnancy. On GD 19, blood pressure was determined and NK cells, mtROS and respiration and AT1\u2010AA production from B cells were measured.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Infusion of IL\u201017 increased blood pressure in the presence or absence of T cells. Mean arterial pressure (MAP) increased with IL\u201017 from 98\u00a0\u00b1\u00a02\u00a0mm Hg (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a012) to 114\u00a0\u00b1\u00a02 (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a012) in SD rats and from 99\u00a0\u00b1\u00a04\u00a0mm Hg (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a07) versus 115\u00a0\u00b1\u00a02\u00a0mm Hg (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a07) in athymic nude rats. Similar trends were seen in NK cells and placental mt ROS. Knowing that IL\u201017 stimulates AT1\u2010AA in SD pregnant rats, we included a group of SD and athymic nude pregnant rats infused with IL\u201017 and the AT1\u2010AA inhibitor peptide (\u2018n7AAc\u2019). The inhibitor attenuated blood pressure (104.9\u00a0\u00b1\u00a03.2,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0=\u00a0.0001) and normalized NK cells and mt function in SD pregnant rats. Importantly, the AT1\u2010AA was not produced in pregnant nude IL\u201017 treated rats, nor did \u2018n7AAc\u2019 effect MAP, in nude athymic rats.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings suggest two conclusions; one is that IL\u201017 causes hypertension and multiorgan dysfunction in the absence of T cells and AT1\u2010AA, possibly through its activation of innate cells and secondly, in the presence of T cells, blockade of the AT1\u2010AA attenuates the effect of IL\u201017. This study indicates the critical effects of elevated IL\u201017 during pregnancy and suggest treatment modalities to consider for PE women.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/aji.13843","type":"journal-article","created":{"date-parts":[[2024,4,12]],"date-time":"2024-04-12T06:38:56Z","timestamp":1712903936000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["The role of T cell stimulated agonistic autoantibodies to the angiotensin II type I receptor (AT1\u2010AA) in mediating multiorgan dysfunction in IL\u201017 induced hypertension during pregnancy"],"prefix":"10.1111","volume":"91","author":[{"suffix":"III","given":"James P.","family":"Hogg","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology University of Mississippi Medical Center  Jackson 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