General obstetrics and gynecologyInterleukin-10 messenger ribonucleic acid in human placenta: Implications of a role for interleukin-10 in fetal allograft protection☆
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2021, Journal of Reproductive ImmunologyEffects of hydroxychloroquine on the human placenta—Findings from in vitro experimental data and a systematic review
2019, Reproductive ToxicologyCitation Excerpt :However, a small but significant reduction in hPL release by HCQ was observed after 72 h; as hPL is essential for a healthy pregnancy, this finding warrants further investigation. Human IL-10 is a cytokine produced by CD4 + T cell clones, B cells and monocytes [44] and is believed to play an important role in the placenta inducing maternal tolerance of the allogeneic fetus [44,45]. Moreau et al. (1999) proposed that IL-10 achieves this by altering the HLA class I expression pattern at the maternal-fetal barrier, thereby protecting the fetus from rejection [46].
Langerhans cell precursors acquire RANK/CD265 in prenatal human skin
2015, Acta HistochemicaInterleukin-10 regulates fetal extracellular matrix hyaluronan production
2013, Journal of Pediatric SurgeryInteraction of pregnancy and autoimmune rheumatic disease
2012, Autoimmunity ReviewsCitation Excerpt :IL-1 β and TNFα are expressed in chorionic villous tissue in the first trimester [56]. Human placenta at term expresses high mRNA levels of IL-10 [57]. Thus cytokine expression at the feto-maternal interface is regulated according to the stage of pregnancy to create optimal conditions for fetal development.
Effect of Interleukin-10 Overexpression on the Properties of Healing Tendon in a Murine Patellar Tendon Model
2008, Journal of Hand SurgeryCitation Excerpt :Evidence also suggests that IL-10 may play a specific anti-inflammatory role during pregnancy. The cytokine is known to be present in amniotic fluid and has been implicated in preventing immune and inflammatory responses to the fetus and fetal “foreign” antigens.39,62,63 The presence of IL-10 may be necessary for scarless fetal wound healing to occur, despite the potential availability of compensatory factors.35
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Supported by National Institutes of Health grant No. 1-R01-D08354-02 (T.K.H.).