Britta Panda

Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack

A critical assessment of the “sterile womb” and “in utero colonization” hypotheses: implications for research on the pioneer infant microbiome

Nucleoside-modified mRNA vaccination partially overcomes maternal antibody inhibition of de novo immune responses in mice

Functional activity but not gene expression of toll-like receptors is decreased in the preterm versus term human placenta

Plasticenta: First evidence of microplastics in human placenta

A proteomic atlas of senescence-associated secretomes for aging biomarker development

REVIEW ARTICLE: Toll‐Like Receptors at the Maternal–Fetal Interface in Normal Pregnancy and Pregnancy Disorders

Inflammation and pregnancy: the role of the immune system at the implantation site

Maternal immunisation: collaborating with mother nature

Resveratrol Reduces the Proinflammatory Effects and Lipopolysaccharide- Induced Expression of HMGB1 and TLR4 in RAW264.7 Cells

Systemic Lupus Erythematosus

Placental origins of adverse pregnancy outcomes: potential molecular targets: an Executive Workshop Summary of the Eunice Kennedy Shriver National Institute of Child Health and Human Development

Pre-eclampsia

Mechanisms of Key Innate Immune Cells in Early- and Late-Onset Preeclampsia

Heparin and maternal fetal interface: Why should it work to prevent pregnancy complications?

DAMPs as mediators of sterile inflammation in aging-related pathologies

Antiphospholipid syndrome

Orthogonal Design of Experiments for Engineering of Lipid Nanoparticles for mRNA Delivery to the Placenta

DAMPening Inflammation by Modulating TLR Signalling

Longitudinal expression of Toll-like receptors on dendritic cells in uncomplicated pregnancy and postpartum

ORIGINAL ARTICLE: Regulation of Nod1 and Nod2 in First Trimester Trophoblast Cells

ORIGINAL ARTICLE: Antiphospholipid Antibodies Induce a Pro‐Inflammatory Response in First Trimester Trophoblast Via the TLR4/MyD88 Pathway

Dendritic cells in the circulation of women with preeclampsia demonstrate a pro-inflammatory bias secondary to dysregulation of TLR receptors