Cytotoxic activity and phenotypic analysis of natural killer cells in early normal human pregnancy

Lee, H.; Gregory, C. D.; Rees, Gareth; Scott, Ian; Golding, P R

doi:10.1016/0165-0378(87)90079-9

Cited by 28 publications

(8 citation statements)

References 13 publications

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“…One possibility was that pregnancy prevented activation of cell types such as NK cells as a perturbation in their peripheral numbers can lead to spontaneous abortion and pre-eclampsia (35)(36)(37). Pregnancy hormones, estrogen, progesterone, and prolactin may have dampening effects on peripheral NK cells (38).…”

Section: Discussionmentioning

confidence: 99%

Pregnancy Impairs the Innate Immune Resistance toSalmonella typhimuriumLeading to Rapid Fatal Infection

Pejčić-Karapetrović

Gurnani

Russell

et al. 2007

The Journal of Immunology

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Typhoid fever and gastroenteritis caused by Salmonella enterica species are increasing globally. Pregnancy poses a high risk, but it is unclear how maternal immunity to infection is altered. In mice, susceptible strains die of S. enterica serovar typhimurium (ST) infection within 7 days whereas resistant mice (129×1/SvJ) develop a chronic infection. We found that virulent ST infection during pregnancy, in normally resistant 129×1/SvJ mice, evoked ∼100% fetal loss and surprisingly >60% host fatality, with a median survival of 6 days. Splenic bacterial load was 1000-fold higher in pregnant mice. This correlated to a diminished splenic recruitment/expansion of innate immune cells: dendritic cells, neutrophils, and NK cells. In particular, the splenic expansion and activation of NK cells postinfection seen in nonpregnant mice was lacking in pregnancy. Most notably, pregnant-infected mice had decreased production of serum IL-12 and increased IL-6 levels. Moreover, uteroplacental tissue of pregnant-infected mice exhibited an ∼40-fold increase in IL-6 mRNA expression relative to noninfected placenta, whereas IL-12p40 was not increased. In vivo blocking of IL-6 significantly reduced the splenic bacterial burden in pregnant mice yet failed to prevent fetal loss. Fetal demise correlated to the rapidity of infection; by 14 h, ST expanded to >105 in the placenta and had reached the fetus. Therefore, the preferential placental expansion of ST plausibly altered the inflammatory response toward IL-6 and away from IL-12, reducing the recruitment/activation of splenic innate immune cells. Thus, highly virulent pathogens may use placental invasion to alter systemic host resistance to infection.

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Section: Discussionmentioning

confidence: 99%

Pregnancy Impairs the Innate Immune Resistance toSalmonella typhimuriumLeading to Rapid Fatal Infection

Pejčić-Karapetrović

Gurnani

Russell

et al. 2007

The Journal of Immunology

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“…During pregnancy, an NK cell depression is present from the first trimester to the postpartum period (875,876). The mechanism of this depression is not clear, and both normal and decreased levels in the numbers of NK cells, in the NK cell cytotoxic potential, and in the recycling ability have been reported (877)(878)(879)(880). The depression of NK cell cytotoxic activity in pregnancy correlates inversely with the level of 170-estradiol in the sera of pregnant women.…”

Section: Nk Cells and Reproductionmentioning

confidence: 99%

Biology of Natural Killer Cells

Trinchieri

1989

Advances in Immunology

2,679

1,717

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“…Healthy non-pregnant women ( n = 18) were recruited from hospital staff, and were of reproductive age (median 30, range 20-45 years), not on any medication and had no history of chronic inflammatory disease, allergy or blood transfusions. Similarly healthy pregnant women ( n = 20) were recruited with informed consent from antenatal clinics (John Radcliffe Hospital and Quarry Surgery, Oxford), with a median age of 30·5 years (range [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37]. All were in the third trimester of pregnancy (median gestation 34 weeks, range [30][31][32][33][34][35][36][37][38][39][40] and not in labour at the time of blood sampling, and progressed normally to term.…”

Section: Subjectsmentioning

confidence: 99%

Monocytes are primed to produce the Th1 type cytokine IL-12 in normal human pregnancy: an intracellular flow cytometric analysis of peripheral blood mononuclear cells

Sacks

Redman

Sargent

2003

Clinical and Experimental Immunology

139

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SUMMARYThis paper considers both monocytes and peripheral blood lymphocytes as potential targets for maternal immunological modulation in pregnancy. Peripheral blood mononuclear cells (PBMCs) from nonpregnant and normal pregnant donors were stimulated in vitro , and cytokine production detected intracellularly by flow cytometry. It was found that monocyte production of TNF-a was unaltered in pregnancy, while production of IL-12 was significantly enhanced. In contrast, production of the Th1 type cytokine IFN-g was suppressed in the lymphocyte subsets: CD4 + T helper cells and CD56 + NK cells. Production of the Th2 type cytokine IL-4 in CD4 + cells was not significantly altered in pregnancy. These data suggest that the concept that pregnancy is a 'Th2 phenomenon' cannot be generalized to the function of all aspects of maternal cellular immunity as, paradoxically, circulating monocytes are 'primed' to produce the Th1 cytokine IL-12. Furthermore, these data support the hypothesis that components of maternal innate immunity are activated in normal pregnancy.Keywords human pregnancy interleukin 12 monocytes Th1/Th2

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Cytotoxic activity and phenotypic analysis of natural killer cells in early normal human pregnancy

Cited by 28 publications

References 13 publications

Pregnancy Impairs the Innate Immune Resistance toSalmonella typhimuriumLeading to Rapid Fatal Infection

Pregnancy Impairs the Innate Immune Resistance toSalmonella typhimuriumLeading to Rapid Fatal Infection

Biology of Natural Killer Cells

Monocytes are primed to produce the Th1 type cytokine IL-12 in normal human pregnancy: an intracellular flow cytometric analysis of peripheral blood mononuclear cells

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