ArticleRetrovirology2012
Placental Hofbauer cells limit HIV-1 replication and potentially offset mother to child transmission (MTCT) by induction of immunoregulatory cytokines.
Article in Retrovirology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 98 citations in OpenAlex.
- Phenotypic and functional characterization of first-trimester human placental macrophages, Hofbauer cells.The Journal of experimental medicine · 2021Trial
- Mechanistic insights into the impact of prenatal viral infections on maternal and offspring immunity.Npj viruses · 2026Review
- Isolation and characterization of Hofbauer cells from human term placentas.Frontiers in immunology · 2026Review
- Distinct immune responses to HIV and CMV in Hofbauer cells across gestation highlight evolving placental immune dynamics.Frontiers in immunology · 2026Article
- Joining the dots: maternal cytomegalovirus, HIV and the placenta.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- FcγRI is the key determinant of antibody-mediated Zika virus infection of human placental macrophages.bioRxiv : the preprint server for biology · 2025Article
- The human placenta and its role in reproductive outcomes revisited.Physiological reviews · 2025Review
- Impact of endocrine disrupting chemicals on macrophages at the maternal-fetal interface.Seminars in immunopathology · 2025Review
- The Complex Role of CD8+ T Cells in Placental HIV Infection.European journal of immunology · 2025Review
- Monkeypox Virus Subverts the Inflammatory Response of Macrophages at the Maternal-Fetal Interface.Journal of medical virology · 2025Article
- TGFβ signalling: a nexus between inflammation, placental health and preeclampsia throughout pregnancy.Human reproduction update · 2024Review
- Vertical Transmission of SARS-CoV-2-Specific Antibodies and Cytokine Profiles in Pregnancy.The Journal of infectious diseases · 2024Article
- Review
- Elevated levels of exogenous prolactin promote inflammation at the maternal-fetal interface via the JAK2/STAT5B signaling axis.Frontiers in immunology · 2024Article
- Immunoexpression of neuropilin-1 in the chorionic villi of HIV-infected preeclamptic South African women of African ancestry.Histochemistry and cell biology · 2023Article
- Placental macrophage responses to viral and bacterial ligands and the influence of fetal sex.iScience · 2022Article
- The Innate Defense in the Zika-Infected Placenta.Pathogens (Basel, Switzerland) · 2022Review
- Isolation of Decidual Macrophages and Hofbauer Cells from Term Placenta-Comparison of the Expression of CD163 and CD80.International journal of molecular sciences · 2022Article
- Transplacental Zika virus transmission in ex vivo perfused human placentas.PLoS neglected tropical diseases · 2022Article
- Host-Viral Interactions at the Maternal-Fetal Interface. What We Know and What We Need to Know.Frontiers · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.