Impairment of the accumulation of decidual T cells, NK cells, and monocytes, and the poor vascular remodeling of spiral arteries, were observed in oocyte donation cases, regardless of the presence or absence of preeclampsia.
In oocyte donation (OD) pregnancies, a fetus is a complete allograft to the maternal host and OD pregnancies are an independent risk factor for preeclampsia. Immunocompetent cells contribute to spiral artery remodeling and the failure of this process could contribute to the pathophysiology of preeclampsia. Recent data have shown that impaired autophagy of extravillous trophoblasts (EVT) may induce poor vascular remodeling in preeclampsia. We have studied the distribution of T cells, NK cells and macrophages in the decidua basalis of 14 normotensive OD pregnancies, 5 preeclamptic OD cases, 16 normotensive pregnancy cases, and 13 preeclamptic cases in natural pregnancy or autologous oocyte IVF-ET (NP/IVF). The populations of decidual CD3(+)T cells, CD8(+)T cells, CD4(+)T cells, Foxp3(+)Treg cells, CD56(+)NK cells, and CD68(+) macrophages in preeclampsia were significantly smaller than those in normal pregnancy in NP/IVF. Those frequencies in normotensive OD pregnancies or preeclamptic cases in OD pregnancies were similar to those in preeclamptic cases in NP/IVF. Impaired vascular remodeling was observed in OD pregnancies, regardless of the presence or absence of preeclampsia. The expression of p62, an impaired autophagy marker in EVT of normotensive or preeclamptic OD pregnancies, was significantly higher than that in normal pregnancies in NP/IVF. Immunological change in the decidua basalis and impairment of autophagy in EVT may induce impairment of spiral artery remodeling in OD pregnancies.
Department of Obstetrics and Gynecology, University of Toyama, Toyama-shi 930-0194, Japan; Department of Obstetrics and Gynecology, Aiiku Hospital, Tokyo 105-8321, Japan.
Yasushi
Y
Nakabayashi
Department of Obstetrics and Gynecology, University of Toyama, Toyama-shi 930-0194, Japan.
Akitoshi
A
Nakashima
Department of Obstetrics and Gynecology, University of Toyama, Toyama-shi 930-0194, Japan.
Osamu
O
Yoshino
Department of Obstetrics and Gynecology, University of Toyama, Toyama-shi 930-0194, Japan.
Tomoko
T
Shima
Department of Obstetrics and Gynecology, University of Toyama, Toyama-shi 930-0194, Japan.
Arihiro
A
Shiozaki
Department of Obstetrics and Gynecology, Aiiku Hospital, Tokyo 105-8321, Japan.
Tomoko
T
Adachi
Department of Obstetrics and Gynecology, Aiiku Hospital, Tokyo 105-8321, Japan.
Masao
M
Nakabayashi
Department of Obstetrics and Gynecology, Aiiku Hospital, Tokyo 105-8321, Japan.
Takashi
T
Okai
Department of Pathology, Showa University Koto Toyosu Hospital, Tokyo 135-8577, Japan.
Miki
M
Kushima
Department of Obstetrics and Gynecology, University of Toyama, Toyama-shi 930-0194, Japan. Electronic address: s30saito@med.u-toyama.ac.jp.
Shigeru
S
Saito
D000328:Adult; D003656:Decidua / Q000276:immunology* / Q000473:pathology; D005260:Female; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology* / Q000473:pathology; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology* / Q000473:pathology; D018587:Oocyte Donation; D011225:Pre-Eclampsia / Q000276:immunology* / Q000473:pathology; D011247:Pregnancy; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D066253:Vascular Remodeling / Q000276:immunology*
Autophagy; Immunomaladaptation; Spiral artery remodeling; Tolerance; Treg