Infection and immunity at the maternal-placental-fetal interface: Focus on HIV-1

Nahmias, André J.; Abramowsky, Carlos R.; Dobronyi, I.; Ibegbu, Chris; Henderson, Sheryl L.

doi:10.1016/s0143-4004(98)80036-2

Cited by 8 publications

(7 citation statements)

References 46 publications

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“…1b,c; right graph). This result is consistent with earlier suggestions 22 that the maternal–fetal interface is supportive of Th2 responses. However, it is likely that there exist more levels of complexity in the immune regulation of the maternal–fetal interface.…”

Section: Resultssupporting

confidence: 93%

Dendritic cells: a family portrait at mid‐gestation

Bizargity

Bonney

2009

Immunology

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Summary Recent advances in our understanding of dendritic cells (DCs) and their role in tolerance and immunity has fuelled study of their normal development and function within the reproductive tract. The common hypothesis that pregnancy is a state of immune suppression or deviation now includes the idea that alterations in DC phenotype and function are critical for maternal tolerance. We chose to study DCs in the uterus and lymphoid tissue in non‐pregnant and pregnant mice at mid‐gestation to understand what DC‐related factors may be involved in premature birth. We used a mouse model where the mother’s immune system has been shown to respond to the male antigen H‐Y. Observed differences among DCs in the uterus, uterine draining nodes and spleen, even in non‐pregnant mice, suggest the existence of a specialized uterus‐specific subset of DCs. We further found that, amongst CD45+ CD11c+ cells in the uterus and peripheral lymphoid tissue of pregnant mice, expression of major histocompatibility complex class II (MHC II) and costimulatory molecules (i.e. CD80) was similar to that in the non‐pregnant state. Moreover, there was no pregnancy‐related decrease in the proportion of CD11c+ cells in the uterus or in the uterine node that were CD11b− CD8+. Pregnancy increased the CD11b+ subsets and the expression of chemokine (C‐C motif) ligand 6 (CCL6) in DCs of the uterine draining nodes. Finally, DC subsets showed variable expression, with respect to tissue and pregnancy, of the cytokine interleukin‐15, which is important in lymphoid cell homeostasis. For DCs, pregnancy is not a state of immune paralysis, but of dynamic developmental change.

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Section: Resultssupporting

confidence: 93%

Dendritic cells: a family portrait at mid‐gestation

Bizargity

Bonney

2009

Immunology

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“…Novel HOX gene adaptations over the past 3 million years have been involved in fetal -placental -maternal immune interactions permitting the fetus not to be rejected or to cause harm to the mother. Such maternal -placental-fetusinfant immune interactions we called the "Great Balancing Act" (Nahmias and Kourtis 1997), as well as factors related to why pregnant women do not reject their fetus (Nahmias et al 1998a), can be better explained now in the context of the HOX gene discoveries. Similarly, the embryology of congenital anomalies of body patterning is now being better understood (Goodman 2003).…”

Section: Our Longtime Search For the "O" Infectious Agents Associatedmentioning

confidence: 99%

The Possible Role of Transplacentally‐Acquired Antibodies to Infectious Agents, With Molecular Mimicry to Nervous System Sialic Acid Epitopes, as Causes of Neuromental Disorders: Prevention and Vaccine Implications

Nahmias

Nahmias²,

Danielsson

2006

Journal of Immunology Research

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Proof of causality of most neuromental disorders (NMD's) is largely unavailable. Lessons from four-decade investigations of the epidemiology, immunology, pathogenesis, prevention and therapy of perinatal infectious agents, which invade directly the nervous system, have led us to propose a new indirect effect hypothesis: maternal transplacentally-acquired antibodies, to agents with epitope molecular mimicry with the developing nervous system, can cross the fetus/infant's blood -nervous system barriers to cause NMD's, clinically manifest years later.Further rationale is provided by relevant evolutionary/developmental (EVO -DEVO) considerations-applicable also to some vaccines. The hypothesis is being tested in: (a) older pregnancy studies with available maternal and newborn sera, and follow-up of the progeny for NMD's; and (b) NMD registry individuals linked to their stored newborn blood spots. Preliminary results support a possible role for schizophrenia of high-tittered antibodies to some agents (toxoplasma, influenza and herpes simplex type 2 virus).A model that includes likely genetic and postnatal influences is schematized and a list of putative agents and factors, based on varying rationales, is tabulated. In case pilot studies are confirmed, the identified agent(s) and antibodies would need to be tested in new prospectively enrolled pregnant women, so as to establish further risk factors leading to possible preventive modalities.

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“…Several studies have demonstrated potential modes of HIV-1 transplacental passage [9,10]. Recently, maternal cells were identified in fetal lymph nodes and noted to induce the development of T regulatory cells that suppress fetal anti-maternal immunity [11].…”

Section: Introductionmentioning

confidence: 99%

Placental Hofbauer cells limit HIV-1 replication and potentially offset mother to child transmission (MTCT) by induction of immunoregulatory cytokines

Johnson

Chakraborty

2012

Retrovirology

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BackgroundDespite readily detectable levels of the HIV-1 (co)-receptors CD4, CCR5 and DC-SIGN on placental macrophages (Hofbauer Cells [HCs]), the rate of HIV-1 infection in utero in the absence of interventions is only 7% of exposed infants. Here, we examine the replication kinetics of human HCs to the primary isolate HIV-1BaL. We also determined the infectivity of HIV-1-exposed HCs by co-culturing with isolated cord and peripheral blood mononuclear cells [CBMCs, PBMCs]. To understand the limiting nature of HCs to HIV-1 replication, we examined the effect of endogenously secreted cytokines on replication kinetics.ResultsHCs have reduced ability to replicate HIV-1 in vitro (p < 0.01) and to transmit virus to CBMCs and PBMCs (p < 0.001 for both) compared to standard infections of MDMs. HCs were shown to release HIV-1 particles at levels comparable to MDMs, however exhibit significant decreases in viral transcription (gag and env), which may account for lower levels of HIV-1 replication. Un-stimulated HCs constitutively express significantly higher levels of regulatory cytokines, IL-10 and TGF-β, compared to MDMs (p < 0.01), which may contribute to immunoregulatory predominance at the placenta and possibly account for down-regulation of HIV-1 replication and infectivity by HCs. We further demonstrate that these regulatory cytokines inhibit HIV-1 replication within HCs in vitro.ConclusionHCs have reduced ability to replicate and disseminate R5-tropic HIV-1BaLin vitro and potentially offset mother to child transmission (MTCT) of HIV-1 by the induction of immunoregulatory cytokines. Despite the potential for migration and infectivity, HCs are not present in the neighboring fetal circulation. These results implicate HCs as important mediators of protection at the feto-maternal interface during ongoing HIV-1 exposure.

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Infection and immunity at the maternal-placental-fetal interface: Focus on HIV-1

Cited by 8 publications

References 46 publications

Dendritic cells: a family portrait at mid‐gestation

Dendritic cells: a family portrait at mid‐gestation

The Possible Role of Transplacentally‐Acquired Antibodies to Infectious Agents, With Molecular Mimicry to Nervous System Sialic Acid Epitopes, as Causes of Neuromental Disorders: Prevention and Vaccine Implications

Placental Hofbauer cells limit HIV-1 replication and potentially offset mother to child transmission (MTCT) by induction of immunoregulatory cytokines

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