Immunobiology of the Feto‐Maternal Interface

Lala, Peeyush K.; Chatterjee‐Hasrouni, Saswati; Kearns, Mary; Montgomery, Barbara; Colavincenzo, V.

doi:10.1111/j.1600-065x.1983.tb01092.x

Cited by 97 publications

(19 citation statements)

References 85 publications

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“…The mechanisms by which the allogeneic fetus circumvents the maternal immune response in the pregnant uterus have been investigated [3,16,17]. The mechanisms by which the allogeneic fetus circumvents the maternal immune response in the pregnant uterus have been investigated [3,16,17].…”

Section: Discussionmentioning

confidence: 99%

Evidence of specialized leukocyte-vascular homing interactions at the maternal / fetal interface

1999

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In normal pregnancy, the maternal immune system fails to reject the fetus or the placenta as an allogeneic graft. We hypothesize that specialized mechanisms of leukocyte recruitment might limit access of circulating maternal immune cells to the maternal/fetal interface. During the critical period of initial trophoblast invasion there is an elegantly orchestrated progression of leukocyte homing events in the decidua basalis, associated with highly regulated expression of vascular addressins and segregation of specialized leukocyte subsets into well-defined decidual microdomains. Neutrophils are limited to the region of necrosis associated with enzymatic digestion at the leading edge of the invading trophoblast, where an almost linear array of maternal blood vessels displays the neutrophil ligand E-selectin. Cells with the phenotype of monocytes but expressing § 4 g 7 integrin are localized in the blood vessels of the specialized "vascular zone", which display the unusual combination of P-selectin (partially associated with platelets) and the § 4 g 7 ligand mucosal vascular addressin-1 (MAdCAM-1). Granulated metrial gland cells (§ 4 + g 7-, probably § 4 g 1 +) constitute a well-defined cluster positioned in the central decidua basalis around venules prominently expressing the § 4 g 1 ligand VCAM-1 (but not MAdCAM-1). T and B lymphocytes are rare. Our results suggest that selective mechanisms for regulating leukocyte access, associated with microdomain specialization within the decidua basalis, may play a fundamental role in immune regulation during the invasive period of placental development.

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Section: Discussionmentioning

confidence: 99%

Evidence of specialized leukocyte-vascular homing interactions at the maternal / fetal interface

1999

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“…The placenta is composed of both fetally-derived trophoblasts and maternally-derived decidual cells. Interestingly, it has been shown (14,15) that at least some of the decidual cells arise from bone marrow precursors . Uterine CSF-1 may also cause local proliferation and differentiation of cells of the mononuclear phagocytic lineage, giving rise to mature macrophages.…”

Section: Discussionmentioning

confidence: 99%

Regulation of colony-stimulating factor 1 during pregnancy.

Bartocci¹,

Pollard²,

Stanley

1986

The Journal of Experimental Medicine

298

124

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Colony-stimulating factor I (CSF-1) is a homodimeric glycoprotein growth has been shown to regulate the survival, proliferation, and differentiation of mononuclear phagocytes (reviewed in 1). Its receptor is a 165 kd tyrosine kinase, closely related or identical to the c-fms protooncogene product (2) .Extensive studies in vitro (1, 3), and preliminary in vivo experiments (E. R. Stanley, and T . R. Bradley, unpublished observations) indicate that CSF-I selectively regulates mononuclear phagocyte production . However, other possible effects of CSF-I were suggested by a study (4) in which high levels of colonystimulating activity were found in pregnant uterus and fetal tissues. Furthermore, recent observations (5) have shown the existence of the CSF-I receptor and the cjms gene product in human choriocarcinoma. cell lines. In this paper, we find that pregnancy induces a 1,000-fold increase in the murine uterine CSF-I concentration, which appears to be regulated by chorionic gonaclotrophin (CG). These observations suggest a novel role for CSF-I in pregnancy . Materials and MethodsEndotoxin-unresponsive 8-12-wk-old C3H/HeJ mice (The Jackson Laboratory, Bar Harbor, ME) were used exclusively . Females were mated, and day zero of pregnancy was

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“…It has become increasingly evident that the primary mechanisms operate locally at the fetomaternal interface (Lala et al, 1983;Clark et al, 1984Clark et al, , 1987. In recent years, the possibility that decidual tissue plays an immunological role in the maintenance of pregnancy has been examined in detail.…”

Section: Introductionmentioning

confidence: 99%

Hemopoietic origin of certain decidual cell precursors in murine pregnancy

et al. 1989

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The possible hemopoietic origin of certain precursors of uterine decidual cells appearing during normal murine pregnancy was investigated in semiallogeneic hemopoietic chimeras with retained or regained fertility. Chimeras were produced by three different methods in two donor-host combinations: F1 [BALB/c female x C3H/HeJ male] cells introduced into the parental strain BALB/c female hosts or F1 [CBA/J female x C57BL/6 male] cells introduced into CBA/J female hosts. Prenatal chimeras (PN) were made by reconstituting mouse fetuses (day 13-17) with 10(6)-10(7) adult bone marrow or fetal liver cells through the yolk sac and they were allowed to be delivered naturally. Neonatal chimeras (NN) were made by injecting 1-2 x 10(7) adult bone marrow cells into the anterior facial vein of neonatal mice (less than 24 hr old). In both cases, experimental animals were raised to maturity. Ovary-transplanted chimeras (OT) were made by injecting 10(7) bone marrow cells into lethally irradiated (9.5 Gy) young adult female mice, followed 6 weeks later with bilateral orthotopic transplants of syngeneic ovary grafts to restore fertility. All female chimeras produced by the three different methods were mated with syngeneic male partners to produce normal pregnancy. The extent of chimerism at the cellular level was determined in all cases by a radioautographic identification of the H-2 phenotype of splenic lymphocytes and decidual cells and macrophages in the collagenase-dispersed decidua at day 11-16 of normal pregnancy, following a sandwich labelling with monospecific anti-H-2 antibodies and 125I-protein A. Morphological discrimination of typical decidual cells from macrophages in the collagenase-dispersed decidua was carried out on the basis of several distinctive markers: presence of surface Dec-1 and Thy-1 and absence of surface F4/80 or latex phagocytosis for decidual cells, in contrast to macrophages which were phagocytic and expressed F4/80 but not Dec-1 or Thy-1. While the degree of hemopoietic chimerism (judged by the incidence of donor-derived lymphocytes in the spleen) varied from animal to animal, in all three groups (PN, NN, and OT) comprising a total of 26 chimeras, the percentage of typical decidual cells expressing donor H-2 phenotype showed an excellent correlation with that for small lymphocytes in the spleen. These results reveal that at least a subpopulation of typical decidual cells of the pregnant uterus has a hemopoietic genealogy. A possible familial relationship of these cells to granulated metrial gland cells remains unclear.

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Immunobiology of the Feto‐Maternal Interface

Cited by 97 publications

References 85 publications

Evidence of specialized leukocyte-vascular homing interactions at the maternal / fetal interface

Evidence of specialized leukocyte-vascular homing interactions at the maternal / fetal interface

Regulation of colony-stimulating factor 1 during pregnancy.

Hemopoietic origin of certain decidual cell precursors in murine pregnancy

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