Immunoregulation of fetal and anti-paternal immune responses

Seavey, Matthew M.; Mosmann, Tim R.

doi:10.1007/s12026-007-8005-x

Cited by 30 publications

(19 citation statements)

References 88 publications

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“…While some essential 1,25(OH) 2 D 3 functions in female fertility relate to reproductive tissue development [262,263], other functions probably relate to immune tolerance induction and are highly relevant to the protective effects of pregnancy in women with MS. The semi-allogeneic, fetal trophoblast cells must invade the uterine decidua to establish the fetal blood supply, but the uterine decidua harbors T lymphocytes capable of recognizing and attacking the fetal tissue bearing paternal antigens [264]. Incompletely understood mechanisms exist at the border between mother and fetus to promote maternal immune tolerance of the fetus without unduly compromising immune responses to infectious agents.…”

Section: Multiple Sclerosis Pregnancy and Immune Tolerancementioning

confidence: 99%

Vitamin D and Multiple Sclerosis

Hayes¹,

Nashold²,

Mayne³

et al. 2011

Vitamin D

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Section: Multiple Sclerosis Pregnancy and Immune Tolerancementioning

confidence: 99%

Vitamin D and Multiple Sclerosis

Hayes¹,

Nashold²,

Mayne³

et al. 2011

Vitamin D

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“…þ T lymphocytes (both ab and gd T cells, with a greater proportion of gd cells), and a subset of lymphocytes, natural killer T (NKT) cells [Dang et al 2000;Hunt 2006;Seavey and Mosmann 2008]. Neutrophils and monocytes circulate throughout the maternal placental vasculature and have been shown to infiltrate areas of infection, damage, or resorption [Girardi 2008;Girardi et al 2003;Rogerson et al 2003].…”

Section: Immunology Of Pregnancymentioning

confidence: 99%

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

Detmar

Jurisicova

2010

Systems Biology in Reproductive Medicine

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Polycyclic aromatic hydrocarbons (PAHs) are released into the environment as a result of incomplete fossil fuel combustion from industrial furnaces, woodburning stoves, and automobile exhaust fumes; however, the primary source of human exposure to these compounds is cigarette smoke. Embryonic and fetal loss after treatment with high doses of PAHs have been well documented in animal studies; however, few studies have addressed the reproductive consequences of long-term, low-level exposure to these chemicals. We previously reported that low doses of PAHs administered to ICR mice over a period of 9 weeks prior to conception resulted in early embryonic resorptions, whereby treated dams lost approximately 50% of their litter. During the course of these studies, we observed greater numbers of infiltrating uterine natural killer (uNK) cells into the placenta of PAH-exposed conceptuses. While exposure to high levels of PAHs has been shown to be immunosuppressive, increasing evidence suggests that chronic, low-dose exposure to PAHs may stimulate immune cells. Thus, we hypothesized that low-dose, chronic PAH exposure in our mouse model is mediating embryonic resorption by hyperstimulating maternal immune cells. In this review of the literature, we outline the rationale of our argument and present preliminary data, focussing upon PAH-mediated alterations in uNK cell dynamics and how these changes may be linked to early embryonic resorptions.

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“…Proper establishment, progress and success of mammalian pregnancy rely on the capability of the maternal immune system to undergo a series of adaptations tending to tolerate the presence of the semi-allogeneic fetus (Robertson and Moldenhauer, 2014;Seavey and Mosmann, 2008). Among others well described immune-mechanisms; our laboratory has demonstrated that pregnancy induces strong modifications in B cell development (Muzzio et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Progesterone and estradiol exert an inhibitory effect on the production of anti-inflammatory cytokine IL-10 by activated MZ B cells

Bommer

Muzzio

Zygmunt

et al. 2016

Journal of Reproductive Immunology

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Please cite this article as: Bommer, I., Muzzio, D.O., Zygmunt, M., Jensen, F., ଝProgesterone and estradiol exert an inhibitory effect on the production of antiinflammatory cytokine IL-10 by activated MZ B cells.Journal of Reproductive Immunology http://dx.doi.org/10. 1016/j.jri.2016.05.008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. 2 AbstractThe main message of this work is the fact that female sex hormones, progesterone and estradiol, whose levels significantly rise during pregnancy, inhibit the production of anti-inflammatory cytokine IL-10 with no apparent effect on pro-inflammatory cytokine TNF-α by activated MZ B cells. This is an important piece of information and helps to better understand how the maternal immune system controls the balance between immune tolerance and immune activation during pregnancy leading to the simultaneously acceptance of the semi-allogeneic fetus and the proper defense of the mother against pathogens during this critical period of time.

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Immunoregulation of fetal and anti-paternal immune responses

Cited by 30 publications

References 88 publications

Vitamin D and Multiple Sclerosis

Vitamin D and Multiple Sclerosis

Embryonic Resorption and Polycyclic Aromatic Hydrocarbons: Putative Immune-mediated Mechanisms

Progesterone and estradiol exert an inhibitory effect on the production of anti-inflammatory cytokine IL-10 by activated MZ B cells

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