Subset Classification of Mouse Uterine Natural Killer Cells by DBA Lectin Reactivity

Paffaro, Valdemar A.; Bizinotto, Marcia C.; Joazeiro, Paulo Pinto; Yamada, Áureo T.

doi:10.1053/plac.2002.0919

Cited by 158 publications

(205 citation statements)

References 33 publications

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“…Stained uNK cells were evaluated at ϫ400 microscopic magnification to estimate the number of cytoplasmic granules and the diameter of each cell. Both of these parameters normally increase as uNK cells mature (21). Approximately 200 -300 morphologically homogeneous uNK cells of each of four distinct subtypes were collected by focal laser melting of the thermoplastic film from the cap onto the individual desired cells using multiple implantation sites for cell harvesting (24).…”

Section: Lcm Of Unk Cells Rna Isolation and Cdna Synthesismentioning

confidence: 99%

“…To identify IM, nongranulated as well as granulated uNK cells in implantation sites from PlGF null mice and their congenic controls, the standard DBA lectin-staining protocol of Paffaro et al was used (21). ExtrAvidin peroxidase conjugate (Sigma-Aldrich) was used to detect bound biotinylated lectin and was revealed with 3,3Ј-diaminobenzidine in TBS with 0.1% hydrogen peroxide.…”

Section: Immunohistochemistry and Lectin Histochemistrymentioning

confidence: 99%

“…Murine uNK cells are extremely localized within implantation sites, appearing only on the mesometrial side of the uterus. Between gestation day (gd)5-11 (20,21), uNK cells proliferate, gain increasing numbers of cytoplasmic granules, and form a transient lymphoid structure known variously as the mesometrial lymphoid aggregate of pregnancy (MLAp), metrial gland, or decidualized mesometrial triangle. This mural structure surrounds the radial branches of the uterine artery as they arborize into the endometrial spiral arteries.…”

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confidence: 99%

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Genetic Deletion of Placenta Growth Factor in Mice Alters Uterine NK Cells

Tayade

Hilchie

et al. 2007

The Journal of Immunology

110

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Placenta growth factor (PlGF; formerly PGF), a vascular endothelial growth factor gene family member, is expressed in human implantation sites by maternal uterine NK (uNK) and fetal trophoblast cells. Lower than normal concentrations of blood and urinary PlGF have been associated with impending onset of pre-eclampsia, a hypertensive disease of late human gestation characterized by limited intravascular trophoblast invasion. In pregnant rodents, delivery of the PlGF antagonist sFlt-1 or S-endoglin induces pre-eclampsia-like lesions. Mice genetically deleted in PlGF reproduce, but neither their implantation sites nor their uNK cell development are described. We combined real-time PCR of endometrium from nonpregnant and gestation day (gd)6–18 C57BL6/J (B6) mice with immunohistology to analyze PlGF expression in normal mouse pregnancy. To estimate the significance of uNK cell-derived PlGF, PlGF message was quantified in mesometrial decidua from pregnant alymphoid Rag2 null/common γ chain null mice and in laser capture-microdissected B6 uNK cells. Histopathologic consequences from PlGF deletion were also characterized in the implantation sites from PlGF null mice. In B6, decidual PlGF expression rose between gd8–16. uNK cells were among several types of cells transcribing PlGF in decidualized endometrium. Immature uNK cells, defined by their low numbers of cytoplasmic granules, were the uNK cells displaying the greatest number of transcripts. PlGF deletion promoted the early differentiation high numbers of binucleate uNK cells (gd8) but had no other significant, morphometrically detectable impact on implantation sites. Thus, in mice, PlGF plays an important role in successful uNK cell proliferation and/or differentiation.

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Section: Lcm Of Unk Cells Rna Isolation and Cdna Synthesismentioning

confidence: 99%

Section: Immunohistochemistry and Lectin Histochemistrymentioning

confidence: 99%

mentioning

confidence: 99%

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Genetic Deletion of Placenta Growth Factor in Mice Alters Uterine NK Cells

Tayade

Hilchie

et al. 2007

The Journal of Immunology

110

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“…Previous studies on E13.5 placentas suggested that uNK cells are separated from the farthest distal trophoblast cells by a considerable distance (5). Because the remodeling of uterine arteries is initiated much earlier during the phase of trophoblast giant cell invasion, we analyzed midsagittal sections of E8.5 conceptuses for the relative distribution of uNK and trophoblast cells, detected by staining with Dolichus biflores agglutinin (DBA) and pancytokeratin, respectively (5,33). At this stage it was obvious that trophoblast cells in the mesometrial decidua were surrounded by large numbers of uNK cells, some of which had infiltrated the ectoplacental cone (Fig.…”

mentioning

confidence: 99%

Paternal MHC expression on mouse trophoblast affects uterine vascularization and fetal growth

Madeja

Yadi²,

Apps³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

149

118

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The mammalian fetus represents a semiallograft within the maternal uterus yet is not rejected. This situation is particularly pronounced in species with a hemochorial type of placentation, such as humans and rodents, where maternal tissues and blood are in direct contact with fetal trophoblast and thus potentially with paternal antigens. The main polymorphic antigens responsible for graft rejection are MHC antigens. In humans the trophoblast cells invading into the decidua have a unique pattern of MHC class I expression characterized by both classical (HLA-C) and nonclassical (HLA-G and HLA-E) molecules. Whether such an unusual MHC repertoire on the surface of trophoblast is a conserved feature between species with hemochorial placentation has not been resolved. Here we demonstrate, using a range of methods, that C57BL/6 mouse trophoblast predominantly expresses only one MHC class I antigen, H2-K, at the cell surface of giant cells but lacks expression of nonclassical MHC molecules. Antigenic disparity between parental MHCs affects trophoblast-induced transformation of the uterine vasculature and, consequently, placental and fetal gowth. Maternal uterine blood vessels were more dilated, allowing for increased blood supply, in certain combinations of maternal and paternal MHC haplotypes, and these allogeneic fetuses and placentas were heavier at term compared with syngeneic controls. Thus, maternal-fetal immune interactions are instrumental to optimize reproductive success. This cross-talk has important implications for human disorders of pregnancy, such as preeclampsia and fetal growth restriction.decidual artery remodeling | uterine natural killer cells

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“…28 Because the uNK cells in these placentas were labeled with Dolichos biflorus agglutinin lectin, we can conclude that the uNK cell population that was quantified is, in fact, the one that expands during pregnancy. 34 Debate continues about whether this uNK cell population is derived from extra-uterine precursors that home to the uterus and differentiate in situ early in pregnancy or whether uNK cell precursors mature outside the uterus and then migrate to the uterus due to hormonal cues like AM.…”

Section: Maternal-derived Am Is Necessary For Successful Implantationmentioning

confidence: 99%

Adrenomedullin and endocrine control of immune cells during pregnancy

Matson

Caron

2014

Cell Mol Immunol

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The immunology of pregnancy is complex and incompletely understood. Aberrant immune activity in the decidua and in the placenta is believed to play a role in diseases of pregnancy, such as infertility, miscarriage, fetal growth restriction and preeclampsia. Here, we briefly review the endocrine control of uterine natural killer cell populations and their functions by the peptide hormone adrenomedullin. Studies in genetic animal models have revealed the critical importance of adrenomedullin dosage at the maternal-fetal interface, with cells from both the maternal and fetal compartments contributing to essential aspects underlying appropriate uterine receptivity, implantation and vascular remodeling of spiral arteries. These basic insights into the crosstalk between the endocrine and immune systems within the maternalfetal interface may ultimately translate to a better understanding of the functions and consequences of dysregulated adrenomedullin levels in clinically complicated pregnancies. Keywords: adrenomedullin; preeclampsia; pregnancy; spiral artery remodeling; uNK cells INTRODUCTION Pregnancy presents a mysterious immunological paradox that is permitted by the complex, unique immunology of the maternalfetal interface. We are only beginning to understand how this very specialized immune 'subsystem' differs from the systemic immune system and thus effectively protects the fetus from maternal rejection. For example, the sizable uterine natural killer (uNK) cell and macrophage populations found during early pregnancy are distinctive in their cell surface markers and functions compared to their peripheral counterparts. 1,2 Understanding the activity and control of these immune cell types will shed light on this immunological paradox and possibly inform the pathophysiology of complications of pregnancy.During the past decade, numerous studies have characterized critical roles for the peptide hormone adrenomedullin (Adm gene; AM protein) in the establishment and maintenance of a healthy pregnancy. Here, we discuss the effects of AM on implantation and placentation, concentrating on the control of the uNK cell population and its subsequent involvement in the process of spiral artery remodeling-a necessary process for the maternal vascular adaptation to pregnancy. Importantly, studies addressing the link between

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Subset Classification of Mouse Uterine Natural Killer Cells by DBA Lectin Reactivity

Cited by 158 publications

References 33 publications

Genetic Deletion of Placenta Growth Factor in Mice Alters Uterine NK Cells

Genetic Deletion of Placenta Growth Factor in Mice Alters Uterine NK Cells

Paternal MHC expression on mouse trophoblast affects uterine vascularization and fetal growth

Adrenomedullin and endocrine control of immune cells during pregnancy

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