Biology subjects

Erny, D.

Publications and source records attributed to Erny, D..

3 recordsLinked to original sources

bioRxiv2026

Postnatal Maturation of Dendritic Epidermal T Cells and Langerhans Cells Follows Distinct Differentiation Trajectories Independent of Microbiota

The mouse epidermis harbors two key resident immune populations--dendritic epidermal T cells (DETCs), a subset of invariant {gamma}{delta} T cells, and Langerhans cells (LCs), specialized tissue-resident macrophages--both of which play critical roles in immune surveillance, barrier integrity, and tissue homeostasis. While the fetal origin of both cell types has been defined, the cellular and molecular mechanisms that govern their postnatal fates following colonization of the epidermis around birth remain incompletely understood. Here, we present a combination of immunophenotyping- and transcriptome-resolved single-cell map of DETC and LC development in the mouse epidermis from late embryogenesis through adulthood. We delineate differentiation trajectories for both cell types, marked by distinct changes in morphology, proliferation, and transcriptional programming. Using mice deficient in {gamma}{delta} T cells, which lack canonical DETCs, we demonstrate that LCs develop independently of canonical DETCs likely due to the presence of {beta}DETCs. Moreover, analysis of germ-free mice and wildlings reveals that the postnatal development of both DETCs and LCs is independent of microbial colonization. Together, our findings define the core principles underlying the establishment of the mouse epidermal immune niche. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=168 SRC="FIGDIR/small/716534v1_ufig1.gif" ALT="Figure 1"> View larger version (47K): org.highwire.dtl.DTLVardef@18088a0org.highwire.dtl.DTLVardef@189e0f2org.highwire.dtl.DTLVardef@10f37d6org.highwire.dtl.DTLVardef@1ad59c_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

bioRxiv2026

Macrophage renewal in the small intestine governs early-life control of streptococci

Group B Streptococcus (GBS) is both a common intestinal colonizer that is transmitted intergenerationally, and a primary cause of neonatal sepsis worldwide. However, the innate immune mechanisms that restrict the pathogen at the intestinal barrier early in life remain poorly understood. Using an enteral GBS-colonization model in infant mice, we found that lamina-propria (LP) macrophages controlled both GBS-colonization densities and invasion in an age-dependent fashion. LP macrophages turnover and differentiation were strongly impacted by topology. In the small intestine, monocytes infiltration of the LP occurred from birth on in response to perinatally acquired microbiota, whereas in the colon it was driven by the weaning reaction. Moreover, macrophages of the small intestine mounted a robust, MyD88-dependent inflammatory response to GBS, while those of the colon remained largely unaffected. Together, these findings demonstrate that region-specific macrophage dynamics early in life critically influence host-pathogen-interactions during GBS-colonization.

immunology↗

bioRxiv2024

Dynamic role of monocytes and meningeal macrophages in bacterial meningoencephalitis

Macrophages in the meninges, especially in the dura mater sheathing the brain from the skull, are involved in the immune defense of the central nervous system (CNS). However, their site-specific origin and function, both in steady state and in bacterial CNS infections are incompletely understood. Using an intravenous model of streptococcal meningoencephalitis that mimics hematogenous dissemination in humans, we found that bacteria accumulated predominantly in the leptomeninges and dura, whereas invasion into the brain parenchyma was rare. However, monocyte infiltration into the leptomeninges and parenchyma strongly correlated with disease severity. In the dura, infection triggered activation and loss of resident macrophages, followed by rapid engraftment of inflammatory monocytes that transiently replenished the dural macrophage niche. Under homeostasis, dural monocytes were supplied independently of CCR2 from adjacent skull bone marrow. In infection, however, this local reservoir was rapidly exhausted, and the markedly increased demand for monocytes required mobilization from peripheral bone marrow sources, revealing context-dependent heterogeneity in monocyte origin. Infection also reshaped ontogeny of this differential monocyte output, with an increase in Monocyte-Dendritic Cell Progenitor - derived monocytes (MDP-Mo). MDP-Mo exhibited enhanced MHC-II expression and persisted in the brain during the resolution phase together with CD4 T cells, suggesting a role in antigen presentation after bacterial clearance. Together, these findings reveal a highly dynamic and compartment-specific remodeling of monocyte ontogeny, recruitment, and differentiation across CNS borders during bacterial meningoencephalitis. These mechanisms may offer opportunities for therapeutic interventions in the future. One Sentence SummaryStreptococcal meningoencephalitis disrupts homeostatic, skull bone marrow-derived monocyte and macrophage trajectories in the dura.

immunology↗