2003
DOI: 10.1016/s1043-4666(03)00220-5
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Preeclamptic women are deficient of interleukin-10 as assessed by cytokine release of trophoblast cells in vitro

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Cited by 67 publications
(34 citation statements)
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“…In PE patients, these vessels undergo minor modifications, with apparent substitution of the media layer cells by invasive trophoblasts, increased apoptosis of trophoblast cells, placental ischemia and loss of vasomotor control. Our results are consistent with the findings of other authors (Moll, Nienartowicz, Hees, Wrobel, & Lenz, 1988;Zhou, Damsky, & Fisher, 1997;Rein et al, 2003;Roberts & Gammill, 2005;Benirschke, Kaufmann, & Baergen, 2006).…”
Section: Immunohistochemistry (Ihc)supporting
confidence: 94%
“…In PE patients, these vessels undergo minor modifications, with apparent substitution of the media layer cells by invasive trophoblasts, increased apoptosis of trophoblast cells, placental ischemia and loss of vasomotor control. Our results are consistent with the findings of other authors (Moll, Nienartowicz, Hees, Wrobel, & Lenz, 1988;Zhou, Damsky, & Fisher, 1997;Rein et al, 2003;Roberts & Gammill, 2005;Benirschke, Kaufmann, & Baergen, 2006).…”
Section: Immunohistochemistry (Ihc)supporting
confidence: 94%
“…IL-10 is directly involved in the repression of TNF-␣ release (14) and was recently shown to control the onset of irreversible septic shock after cecal ligation and puncture (19,42). IL-10 deficiency has been observed in a vast amount of inflammatory conditions including endotoxemia (9), inflammatory bowel disease (35), peritonitis (6), preeclampsia (25), and psoriasis (22), pointing to a role for IL-10 as a general control factor against inflammatory outburst.…”
mentioning
confidence: 99%
“…In cases of preeclampsia, there is an alteration in the balance between Th1 and Th2-type responses. By contrast, patients with preeclampsia have been shown to have higher levels of serum pro-inflammatory [15,16] and lower levels of anti-inflammatory cytokines [17] compared with healthy pregnant, thereby featuring a Th1-type predominance. Elevated levels of pro-inflammatory cytokines (TNF-α) or their inducers (IL-12) are also supported this activated Th1-type response [9,10,18].…”
Section: Discussionmentioning
confidence: 99%