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  1. Artikel ; Online: A Comprehensive Profile of Chemokine Gene Expression in the Tissues of the Female Reproductive Tract in Mice.

    Menzies, Fiona M / Oldham, Rachel S / Waddell, Carolann / Nelson, Scott M / Nibbs, Robert J B

    Immunological investigations

    2019  Band 49, Heft 3, Seite(n) 264–286

    Abstract: Homeostatic leukocyte trafficking into and within the female reproductive tract (FRT) contributes to fertility and reproductive health. It is unclear how this process is regulated in the anatomically distinct reproductive tissues, or whether the genes ... ...

    Abstract Homeostatic leukocyte trafficking into and within the female reproductive tract (FRT) contributes to fertility and reproductive health. It is unclear how this process is regulated in the anatomically distinct reproductive tissues, or whether the genes involved are affected by cyclical changes in reproductive hormones. In tissues such as skin and intestine, mouse studies have defined evolutionarily conserved molecular mechanisms for tissue-specific homing, interstitial positioning, and leukocyte egress. Chemokine family members are invariably involved, with the chemokine expression profile of a tissue regulating leukocyte content. Reproductive tissues (ovary, vagina, cervix, uterine horn) of 8 week old virgin female C57BL/6 mice (
    Mesh-Begriff(e) Animals ; Chemokines/genetics ; Estrous Cycle/immunology ; Female ; Gene Expression Profiling ; Genitalia, Female/cytology ; Genitalia, Female/metabolism ; Leukocytes/metabolism ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/metabolism ; Organ Specificity/immunology
    Chemische Substanzen Chemokines
    Sprache Englisch
    Erscheinungsdatum 2019-08-20
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 632565-8
    ISSN 1532-4311 ; 0882-0139
    ISSN (online) 1532-4311
    ISSN 0882-0139
    DOI 10.1080/08820139.2019.1655573
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Atypical chemokine receptor ACKR2 mediates chemokine scavenging by primary human trophoblasts and can regulate fetal growth, placental structure, and neonatal mortality in mice.

    Teoh, Pek Joo / Menzies, Fiona M / Hansell, Chris A H / Clarke, Mairi / Waddell, Carolann / Burton, Graham J / Nelson, Scott M / Nibbs, Robert J B

    Journal of immunology (Baltimore, Md. : 1950)

    2014  Band 193, Heft 10, Seite(n) 5218–5228

    Abstract: Inflammatory chemokines produced in the placenta can direct the migration of placental leukocytes using chemokine receptors that decorate the surface of these cells. Fetal trophoblasts can also express receptors for inflammatory chemokines, and they are ... ...

    Abstract Inflammatory chemokines produced in the placenta can direct the migration of placental leukocytes using chemokine receptors that decorate the surface of these cells. Fetal trophoblasts can also express receptors for inflammatory chemokines, and they are one of the few cell types that express atypical chemokine receptor 2 (ACKR2), previously known as D6. ACKR2 binds many inflammatory CC chemokines but cannot stimulate cell migration or activate signaling pathways used by conventional chemokine receptors. Existing evidence suggests that ACKR2 is a specialized chemokine scavenger, but its function in primary human trophoblasts has not been explored. In mice, ACKR2 is thought to be dispensable for the reproductive success of unchallenged females that have conceived naturally, but it can suppress inflammation-induced abortion and aid the survival of implanted allogeneic embryos. In this article, we demonstrate that cultured primary human trophoblasts express ACKR2 far more strongly than genes encoding conventional receptors for inflammatory CC chemokines. Moreover, these cells are capable of the rapid internalization and efficient scavenging of extracellular chemokine, and this is mediated by ACKR2. We also report that in unchallenged DBA/1j mice, Ackr2 deficiency increases the incidence of stillbirth and neonatal death, leads to structural defects in the placenta, and can decrease fetal weight. Loss of Ackr2 specifically from fetal cells makes a key contribution to the placental defects. Thus, primary human trophoblasts use ACKR2 to scavenge chemokines, and ACKR2 deficiency can cause abnormal placental structure and reduced neonatal survival.
    Mesh-Begriff(e) Animals ; Animals, Newborn ; Chemokine CCL2/genetics ; Chemokine CCL2/immunology ; Chemokine CCL26 ; Chemokines, CC/genetics ; Chemokines, CC/immunology ; Female ; Fetal Development ; Fetus ; Gene Expression Regulation, Developmental ; Humans ; Infant ; Longevity ; Mice ; Mice, Inbred DBA ; Mice, Knockout ; Placenta/immunology ; Placenta/metabolism ; Placenta/pathology ; Pregnancy ; Primary Cell Culture ; Receptors, Chemokine/deficiency ; Receptors, Chemokine/genetics ; Receptors, Chemokine/immunology ; Signal Transduction ; Trophoblasts/immunology ; Trophoblasts/metabolism ; Trophoblasts/pathology
    Chemische Substanzen ACKR2 protein, human ; Ackr2 protein, mouse ; CCL2 protein, human ; CCL26 protein, human ; CCL3L1 protein, human ; Chemokine CCL2 ; Chemokine CCL26 ; Chemokines, CC ; Receptors, Chemokine
    Sprache Englisch
    Erscheinungsdatum 2014-10-08
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1401096
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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