Progesterone and estradiol suppress human mononuclear cell cytotoxicity

Feinberg, Bruce B.; Tan, Nenita S.; Walsh, Scott W.; Brath, Peter C.; Gonik, Bernard

doi:10.1016/0165-0378(92)90020-5

Cited by 18 publications

(4 citation statements)

References 24 publications

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“…Therefore, it is likely that PGE 2 synthesized by the luteal cells in this culture system can also inhibit luteal cell-stimulated T lymphocyte proliferation. However, previous studies [12,[23][24][25][26] have demonstrated an inhibitory effect of progesterone on lymphocyte proliferation in several species, including the cow, and in the present study, exogenous progesterone does-dependently inhibited luteal cell-stimulated T lymphocyte proliferation. The inhibitory effect of progesterone on T lymphocyte proliferation in the present study does not appear to be mediated via progesterone receptors in T lymphocytes, because progesterone-receptor mRNA was not detected by RT-PCR in total RNA isolated from PBMCs, which are rich in T lymphocytes.…”

Section: Discussioncontrasting

confidence: 63%

Effects of Prostaglandin F2α and Progesterone on the Ability of Bovine Luteal Cells to Stimulate T Lymphocyte Proliferation1

Cannon

Petroff

Pate

2003

Biology of Reproduction

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Bovine luteal cells express class I and II major histocompatibility complex molecules and stimulate T lymphocyte proliferation in vitro. Proliferation of T lymphocytes is greater in cocultures of luteal cells and T lymphocytes collected following administration of a luteolytic dose of prostaglandin (PG) F2alpha to the cow. Whether this results from changes in luteal cells that increase their ability to stimulate T lymphocyte proliferation or from changes in T lymphocytes that enhance their ability to respond to luteal cells is unclear. To determine which is the case, luteal cell-T lymphocyte cocultures were performed using luteal cells and T lymphocytes isolated from the same animals before and 8 h after administration of PGF2alpha. In the presence of T lymphocytes collected before PGF2alpha administration, luteal cells isolated after PGF2alpha were more potent stimulators of T lymphocyte proliferation than were luteal cells collected before PGF2alpha (P<0.05). The effect of progesterone on luteal cell-stimulated T lymphocyte proliferation was also evaluated. Proliferation of T lymphocytes was greater (P<0.05) in cultures containing the cytochrome P450 side-chain cleavage enzyme-inhibitor aminoglutethimide. Exogenous progesterone caused a dose-dependent inhibition of luteal cell-stimulated T lymphocyte proliferation (P<0.05). Progesterone-receptor mRNA was undetectable in peripheral blood mononuclear cells collected before and after PGF2alpha administration, indicating that the effect of progesterone was not mediated via progesterone receptors in lymphocytes. These results imply that specific changes in luteal cells in response to PGF2alpha enhance the ability of these cells to stimulate T lymphocyte proliferation. These results also demonstrate that progesterone can suppress luteal cell-stimulated T lymphocyte proliferation.

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Section: Discussioncontrasting

confidence: 63%

Effects of Prostaglandin F2α and Progesterone on the Ability of Bovine Luteal Cells to Stimulate T Lymphocyte Proliferation1

Cannon

Petroff

Pate

2003

Biology of Reproduction

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“…This finding is consistent with a previous report from our laboratory, which demonstrated that progesterone downregulates iNOS in uterine mast cells (Huang et al, 1995), as well as the observation that progesterone inhibits the ability of macrophages to kill target cells (Feinberg et al, 1992 …”

Section: Studies Conducted In Vivosupporting

confidence: 83%

Hormonal Regulation of Uterine Macrophages

Hunt

Miller

Platt

1997

Journal of Immunology Research

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Macrophages are major cellular inhabitants of cycling and pregnant mammalian uteri. Their densities and patterns of tissue distribution in this organ fluctuate in concert with levels of circulating female sex steroid hormones, estrogens and progesterone, and their production of various effector molecules also may be hormonally regulated. Hormonal control may be achieved by direct binding to receptors or by indirect pathways where hormones modulate production of various autocrine and paracrine cytokines and growth factors that then target to resident macrophages and influence their secretory profiles. In this paper, we marshall evidence supporting the concept that progesterone acts as a powerful negative regulator of these versatile cells, reducing their migration into the uterus and impairing their ability to produce potent effector molecules such as nitric oxide that could interfere with the success of pregnancy.

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“…Receptors for EGF, CSF-1, IL-6, TNF are present on the trophoblast surface (331,256,14,260), and have been demonstrated to regulate trophoblast growth and differentiation (256,5,110). In addition, placental steroids (progesterone and estrogen) have anti-inflammatory and immunosuppressive properties, and may contribute to some non-specific immunosuppression (301,96), although additional immunosuppressive mechanisms seem to be ofgreater importance (160): Most current reports on the subject focus on the evasive strategies ofthe placenta, and in particular, the trophoblasts. These cells selectively express membrane antigens: syncytiotrophoblasts do not express classical MHC antigen (95,324,370), and will therefore not trigger T cell mediated immune responses (309).…”

Section: Some Immunobioiogical Aspects Ofpiacentamentioning

confidence: 99%

Human placental Fcγ‐binding proteins in the maternofetal transfer of IgG

Kristoffersen

1996

APMIS

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Progesterone and estradiol suppress human mononuclear cell cytotoxicity

Cited by 18 publications

References 24 publications

Effects of Prostaglandin F2α and Progesterone on the Ability of Bovine Luteal Cells to Stimulate T Lymphocyte Proliferation1

Effects of Prostaglandin F2α and Progesterone on the Ability of Bovine Luteal Cells to Stimulate T Lymphocyte Proliferation1

Hormonal Regulation of Uterine Macrophages

Human placental Fcγ‐binding proteins in the maternofetal transfer of IgG

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