bioRxiv Science⌕ Search

bioRxiv · 10.1101/2025.11.24.690260

Quantifying maternal antibody transfer to colostrum and cord blood reveals virus-specific selectivity in dogs

Abstract

BackgroundNeonatal infections are a leading cause of mortality in dogs, with up to 30% of puppies dying within the first three weeks of life. During this period of immune development, protection is highly dependent on maternal antibodies (MatAbs) transferred across the placenta and via colostrum. Despite the critical importance of this transfer, little is known about the biological or clinical factors that determine its magnitude, whether specific antibodies are preferentially transferred, or how these processes vary across a broad population of dogs. MethodsTo quantify and explore the determinants of MatAb transfer in dogs, we analyzed matched maternal serum, cord blood, and colostrum samples collected from 44 client-owned dams undergoing cesarean section at a university veterinary hospital. Total IgG and virus-specific antibodies against canine parvovirus (CPV) and canine distemper virus (CDV) were analyzed. We also evaluated the influence of maternal factors, including age, breed, body weight, parity and litter size on MatAb transfer efficiency. ResultsAcross this diverse population, we observed limited transplacental transfer of MatAbs (4.5-6% maternal titer), in agreement with previous studies and as expected with the endotheliochorial placenta of dogs. In contrast, virus-specific IgG was highly enriched in colostrum, with 10.7-fold (CPV) and 8.1-fold (CDV) increases relative to serum. Transfer efficiency was significantly greater for virus-specific antibodies than for total IgG (3.2-fold), suggesting selective enrichment of antiviral antibodies during colostrogenesis. Maternal serum antibody titer emerged as the primary factor influencing the efficiency of antibody transfer. ConclusionsThese findings provide the most comprehensive quantification to date of MatAb transfer routes in dogs, revealing preferential transfer of virus-specific IgG to colostrum and highlighting the crucial role of colostrum intake for neonatal immunity. This work establishes a foundation for identifying antibody characteristics that influence MatAb transfer efficiency and reiterates the importance of ensuring dams have adequate titers of virus-specific IgG prior to breeding.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Teh, S., Truyen, L. H., Woodyear, S., Palmeri, J., Pimeta-Pereira, A. A., Peprah, A. A., Lanman, E., Lonergan, T., Reid, A. M., Cheong, S. H., caddy, S. L.. 2025-11-27. Quantifying maternal antibody transfer to colostrum and cord blood reveals virus-specific selectivity in dogs. https://doi.org/10.1101/2025.11.24.690260

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Common viral infections seed regionally distinct resident memory T cells in the human CNS

T cells persist in the central nervous system (CNS) and can drive both protection and neurological disease. How these cells are organized in humans and what they recognize is largely unknown. Here, we profiled CD8 T cells across anatomically distinct CNS regions, obtained through on-site autopsies and temporal lobe resection surgeries, using single-cell RNA sequencing, paired T cell receptor sequencing, and DNA-barcoded tetramers. Resident memory T cells (TRM) specific for Epstein-Barr virus, cytomegalovirus, influenza A, and SARS-CoV-2 were identified across CNS compartments. Anatomical location was the strongest correlate of TRM cell state, with leptomeningeal cells adopting a cytokine-poised TRM program, whereas brain TRM cells were transcriptionally restrained. Cells of the same clonotype spanned tissues yet adopted local transcriptional states. Viral specificity added another layer of TRM heterogeneity with GZMK/GZMA-expressing EBV-specific populations and interferon-stimulated gene signatures in SARS-CoV-2 and Influenza A-specific cells. The human CNS thus harbors regionally distinct CD8+ TRM shaped by common viral exposures.

immunology↗

A regulatory T cell signature provides a shared molecular basis for the therapeutic window of opportunity in rheumatic disease

Rheumatic diseases, including rheumatoid arthritis (RA), spondyloarthritis (SpA) and osteoarthritis (OA), show distinct phenotypes yet respond to overlapping therapies, implicating shared immune mechanisms. In the Transimmunom cohort, we profiled peripheral blood from 240 individuals (47 healthy, 44 OA, 91 RA, 58 SpA) across deep immunophenotyping, immunoproteomics and Treg-Teff transcriptomics. Single-layer analyses revealed broader Treg than Teff remodeling, along with a shared pattern of reduced activated Tregs and expanded Helios+ Tregs across all diseases, alongside a decrease in functional Treg subpopulations, including CTLA4+ and CD45RA- Tregs. In RA specifically, LAG3+ Tregs were also expanded. Combining omics layers outperformed single-layer approaches for disease classification. Among individual layers, Treg transcriptomes were most discriminative, and integration uncovered disease-specific programs. Unsupervised clustering identified a cross-disease cluster independent of activity, treatment and age, mapping to early disease (<= years) and dominated by a Treg dysfunction-associated program. These results provide a biological rationale for the therapeutic "window of opportunity" concept and duration-stratified Treg-directed trials.

immunology↗

Inhibitory Fc Receptor sets a time limit on macrophage response to IgG

Antibodies engage both activating Fc Receptors and the inhibitory receptor Fc{gamma}RIIB. Why macrophages need a dedicated inhibitory receptor rather than simply tuning activating receptor signaling is unclear. Using DNA-based chimeric receptors and in silico modeling, we independently controlled activating and inhibitory Fc Receptors. We found that Fc{gamma}RIIB imposed a time limit on macrophage phagocytosis and ERK signaling. The time limit is due to activating Fc Receptors converting PI(4,5)P2 to PI(3,4,5)P3, which is subsequently converted to PI(3,4)P2 by Fc{gamma}RIIB. This leads to a pulse of active signaling, which is sufficient for phagocytosis of small bacteria-sized targets but not phagocytosis of large targets and TNF secretion. Unlike engaging Fc{gamma}RIIB, reducing activating Fc Receptor signaling decreased initiation of phagocytosis, the speed of PI(3,4,5)P3 generation, and the amplitude of ERK signaling. Our results demonstrate that Fc{gamma}RIIB controls the duration of IgG signaling, while the activating Fc Receptors control sensitivity.

immunology↗