T‐cell Tolerance to the Developing Equine Conceptus

Antczak, Douglas F.

doi:10.1111/j.1439-0531.2012.02101.x

Cited by 10 publications

(8 citation statements)

References 90 publications

(161 reference statements)

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“…In the various species that have been studied for MHC antigen expression in the placenta, most trophoblast cell populations downregulate expression of both MHC class I and MHC class II molecules (95). Why express only MHC class I molecules, and why only on the most invasive trophoblast cells?…”

Section: Fetal-maternal Signaling and Placental Evolutionmentioning

confidence: 99%

The Equine Endometrial Cup Reaction: A Fetomaternal Signal of Significance

Antczak

Mestre

Wilsher³

et al. 2013

Annu. Rev. Anim. Biosci.

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A remarkable feature of equine pregnancy is the development of the invasive trophoblast of the chorionic girdle and its formation of the gonadotrophin-secreting endometrial cup cells in early gestation. The details of this process have been revealed only slowly over the past century, since the first description of the endometrial cups in 1912. This centennial presents an opportunity to review the characteristics of the cells and molecules involved in this early, critical phase of placentation in the mare. The invasiveness of the chorionic girdle trophoblast appears to represent an atavistic attribute more commonly associated with the hemochorial placentae of primates and rodents but not with the more recently derived epitheliochorial placentae of the odd-toed ungulates. The nature of and raison d’etre for the strong fetal signals transmitted to the mare by the endometrial cup reaction, and her responses to these messages, are the subject of the present review.

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Section: Fetal-maternal Signaling and Placental Evolutionmentioning

confidence: 99%

The Equine Endometrial Cup Reaction: A Fetomaternal Signal of Significance

Antczak

Mestre

Wilsher³

et al. 2013

Annu. Rev. Anim. Biosci.

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“…In particular, while pregnancy outcomes have been extensively characterized using rodent infection models, the discordance in pregnancy kinetics and immune cell development between rodents and humans limits the translational relevance of these findings, especially for complications related to birth timing (Bezold, et al 2013, Mold and McCune 2012). These limitations are somewhat bypassed in larger mammals including elegant descriptions of pregnancy in horses, sheep, and non-human primates (Antczak 2012, Barry, et al 2006, Jobe 2005, Noronha and Antczak 2010). However, the significantly more prolonged gestation time, relative lack of immunological tools and defined inbred strains, differences in placental architecture, and exponentially higher experimental costs impose other restrictions that are perhaps even more formidable.…”

Section: Infection Induced Shifts In Treg Suppression and Pregnancy Cmentioning

confidence: 99%

Regulatory T cells and the immune pathogenesis of prenatal infection

Rowe¹,

Ertelt²,

Luo³

et al. 2013

Reproduction

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Pregnancy in placental mammals offers exceptional comprehensive benefits of in utero protection, nutrition, and elimination of metabolic waste for the developing fetus. However, these advantages also require durable strategies to mitigate maternal rejection of fetal tissue expressing foreign paternal antigens. Since the initial postulate of expanded maternal immune tolerance by Sir Peter Medawar 60 years ago, an amazingly elaborate assortment of molecular and cellular modifications acting both locally at the maternal placental interface and systemically have been shown to silence potentially detrimental maternal immune responses. In turn, simultaneously maintaining host defense against the infinite array of potential pathogens during pregnancy is equally important. Fortunately, resistance against most infections is preserved seamlessly throughout gestation. On the other hand, recent studies on pathogens with unique predisposition for prenatal infection have uncovered distinctive holes in host defense associated with the reproductive process. Using these infections to probe the response during pregnancy, the immune suppressive regulatory subset of maternal CD4 T cells has been increasingly shown to dictate the inter-workings between prenatal infection susceptibility and pathogenesis of ensuing pregnancy complications. Herein, the recent literature suggesting a necessity for maternal regulatory T cells in pregnancy induced immunological shifts that sustain fetal tolerance is reviewed. Additional discussion is focused on how expansion of maternal regulatory T cell suppression may become exploited by pathogens that cause prenatal infection, and the perilous potential of infection induced immune activation that may mitigate fetal tolerance and inadvertently inject hostility into the protective in utero environment.

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“…The maternal immune system 'is aware' of the fetus, but does not reject it. 7,8 Regulatory T cells (Treg) represent a subpopulation of T cells that suppresses the immune response at different levels. 5 The aim of this process was a closely regulated trophoblast invasion with a concurrent maternal immune tolerance to the semi-allogenic fetus.…”

Section: Introductionmentioning

confidence: 99%