A study on the density and distribution of uterine Natural Killer cells at mid pregnancy in mice genetically-ablated for CCR2, CCR 5 and the CCR5 receptor ligand, MIP-1α

Chantakru, Sirirak; Kuziel, William A.; Maeda, Nobuyo; Croy, B. Anne

doi:10.1016/s0165-0378(00)00076-0

Cited by 67 publications

(38 citation statements)

References 40 publications

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“…Role of CCR2 in lung NK cell influx and outcome of infection. Because CCR2, the only known signaling receptor for MCP-1/CCL2, is expressed on NK cells (34)(35)(36)(37)(38)(39), we sought to corroborate our findings by examining the role of CCR2 on the recruitment of NK cells to the lung in this infection. We first injected CFSE-labeled NK cells from either WT or CCR2 -/-animals into neutrophil-depleted WT or CCR2 -/-mice before inoculation with A. fumigatus (Figure 6a).…”

Section: Effect Of Neutralization Of Mcp-1/ccl2 On the Influx Of Leukmentioning

confidence: 84%

Chemokine-mediated recruitment of NK cells is a critical host defense mechanism in invasive aspergillosis

Morrison

Park²,

Mooney³

et al. 2003

J. Clin. Invest.

189

143

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Section: Effect Of Neutralization Of Mcp-1/ccl2 On the Influx Of Leukmentioning

confidence: 84%

Chemokine-mediated recruitment of NK cells is a critical host defense mechanism in invasive aspergillosis

Morrison

Park²,

Mooney³

et al. 2003

J. Clin. Invest.

189

143

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“…These observations suggest potential roles of MCP-1, MIP-1␣, and RANTES in leukocyte recruitment to the pregnant uterus. However, it is very surprising that normal recruitment of peripheral NK cells was observed in the decidua of mice in which CCR2 (sole signaling receptor for MCP-1), CCR5 (a receptor for both MIP-1␣ and RANTES), and MIP-1␣ were knocked out (25); thus, these molecules probably play a pivotal role in intradecidual organization and the retention of various cell types in the decidua, but are less important in the preferential migration of the decidual NK cells. Therefore, there may be other chemokines and their ligands involved in the preferential accumulation of CD56 bright CD16 Ϫ NK cells in the decidua.…”

Section: Discussionmentioning

confidence: 99%

Human First-Trimester Trophoblast Cells Recruit CD56brightCD16− NK Cells into Decidua by Way of Expressing and Secreting of CXCL12/Stromal Cell-Derived Factor 1

Jin

Yuan

et al. 2005

The Journal of Immunology

157

121

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More than 70% of decidual lymphocytes are NK cells characterized by CD56brightCD16− phenotype, but the mechanisms by which these NK cells are recruited in the decidua are still almost unrevealed. In this study, we first analyzed the transcription of 18 chemokine receptors in the first-trimester decidual CD56brightCD16− NK cells. Among these receptors, CXCR4 and CXCR3 were found highly transcribed, and the expression of CXCR4 was verified in most of the decidual CD56brightCD16− NK cells by flow cytometry. The first-trimester human trophoblasts were found expressing CXCL12/stromal cell-derived factor 1, the specific ligand of CXCR4, by way of in situ hybridization and immunohistochemistry. The primary cultured trophoblast cells were also found to secrete stromal cell-derived factor 1α spontaneously, and its concentration was 384.6 ± 90.7 pg/ml after the trophoblast cells had been cultured for 60 h. All of the ligands for CXCR3 were below the minimal detectable concentration when trophoblast cells were cultured for up to 48 h. Both recombinant human SDF-1α and supernatants of the cultured trophoblast cells exhibited chemotactic activity on decidual CD56brightCD16− NK cells. Our findings suggest that human first-trimester trophoblast cells produce CXCL12, which in turn chemoattracts decidual CD56brightCD16− NK cells. This activity could contribute to the recruitment mechanism of decidual lymphocytes, especially CD56brightCD16− NK cells, in decidua, and may be used at a local level to modulate the immune milieu at the materno-fetal interface.

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“…Decidual cells are known to produce various factors including IL-15, TGF-β, HGF and extracellular matrix that regulate the maternal placenta development [6,7,8]. On the other hand, uterine NK (uNK) cells, specific lymphocytes found throughout pregnancy, differentiate with the progress of placental development and are known to have significant function in the maintenance of pregnancy through stimulating angiogenesis in the placenta [9,10]. The uNK cells differentiate in situ from bone marrow-derived precursor cells that are small and agranular [11,12].…”

mentioning

confidence: 99%

IGF-I Overexpression Causes Fetal Loss during Placentation in Mice

Nakamura

Hondo

Namba

et al. 2004

Journal of Reproduction and Development

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Abstract.To understand the role of IGF-I in murine pregnancy, we studied the reproductive performance of IGF-I overexpressed mice. Fetal loss occurred only in the transfected uterine horn during Day 10-15 of pregnancy. The placenta appeared healthy until Day 10 of pregnancy. From Day 12, the decidua basalis of the transfected horn increased in thickness. The vascular lumen was expanded, and most of embryos were dead. Uterine Natural Killer cells did not undergo apoptosis from Day 10 to Day 15 when they usually go through apoptosis. Thus, it is likely that IGF-I plays a role in the decidual formation through regulation of uNK cells. This is the first report to demonstrate that IGF-I overexpression can cause fetal loss during murine placentation.

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A study on the density and distribution of uterine Natural Killer cells at mid pregnancy in mice genetically-ablated for CCR2, CCR 5 and the CCR5 receptor ligand, MIP-1α

Cited by 67 publications

References 40 publications

Chemokine-mediated recruitment of NK cells is a critical host defense mechanism in invasive aspergillosis

Chemokine-mediated recruitment of NK cells is a critical host defense mechanism in invasive aspergillosis

Human First-Trimester Trophoblast Cells Recruit CD56brightCD16− NK Cells into Decidua by Way of Expressing and Secreting of CXCL12/Stromal Cell-Derived Factor 1

IGF-I Overexpression Causes Fetal Loss during Placentation in Mice

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