Biology subjects

Taylor, J. T.

Publications and source records attributed to Taylor, J. T..

4 recordsLinked to original sources

bioRxiv2025

Childhood brain tumours instruct cranial haematopoiesis and immunotolerance

Recent research has revealed a remarkable role for immunosurveillance in healthy and diseased brains, dispelling the notion that this organ is a passive immune-privileged site1-3. Better understanding of how this immunosurveillance operates could improve the treatment of neurological diseases. Here, using a novel genetically engineered mouse model of ZFTA-RELA ependymoma4-a childhood brain tumour-we characterised an immune circuit between the tumour and antigen presenting, haematopoietic stem/progenitor cells (HSPCs) in the skull bone marrow. The presentation of antigens in the cerebrospinal fluid (CSF) by HSPCs to CD4+ T cells, biased HSPC lineages toward myelopoiesis and polarised CD4+ T-cells to regulatory T cells (T- regs), culminating in tumour immunotolerance. Remarkably, a single infusion of antibodies directed against cytokines enriched in the CSF of mice bearing ZFTA-RELA ependymomas, choroid plexus carcinomas or Group-3 medulloblastoma-all aggressive childhood brain tumours-disrupted this process and caused profound tumour regression. These data unmask a mechanism by which skull bone marrow-derived HSPCs and CD4+ T cells cooperate to promote the immunotolerance of childhood brain tumours. Antibodies that disrupt this immunosurveillance could prove an effective therapy for these cancers that are less toxic than current treatments.

immunology↗

bioRxiv2025

Evaluating sampling strategies for the detection of avian influenza viruses in the environment

Highly pathogenic avian influenza (HPAI) viruses threaten humans, livestock and wildlife, highlighting the urgent need for early warning surveillance. Environmental RNA (eRNA) monitoring provides a safer, cost-effective and non-invasive alternative to direct pathogen testing, yet the effectiveness of different sample types for avian influenza viruses (AIVs) is unclear. We evaluated four eRNA-based sampling methods in urban waterfowl ponds over approximately one year. All methods combined with RT-qPCR and metagenomic sequencing detected AIV, but detections were asynchronous, likely reflecting low viral concentrations or detection limits. These results highlight both the promise and the current limitations of eRNA-based AIV surveillance. Graphic abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=156 SRC="FIGDIR/small/677014v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@e8e189org.highwire.dtl.DTLVardef@12f17fforg.highwire.dtl.DTLVardef@d09f5forg.highwire.dtl.DTLVardef@8f55fd_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

bioRxiv2021

A class I hydrophobin in Trichoderma virens influences plant-microbe interactions through enhancement of enzyme activity and MAMP recognition

The filamentous fungus, Trichoderma virens, is a well-known mycoparasitic plant symbiont, valued for its biocontrol capabilities. T. virens initiates a symbiotic relationship with a plant host through the colonization of its roots. To achieve colonization, the fungus must communicate with the host and evade its innate defenses. Hydrophobins from Trichoderma spp. have previously been demonstrated to be involved in colonization of host roots. In this study, the class I hydrophobin, HFB9A from T. virens was characterized for a potential role in root colonization. {Delta}hfb9a gene deletion mutants colonized less than the wild-type strain, were unable to induce systemic resistance against Colletotrichum graminicola, and showed a reduction in the activity of its cell wall degrading enzymes. The purified HFB9A protein was able to complement the enzyme activity of mutant culture filtrates as well as enhance the activity of commercially sourced cellulase. When exogenously applied to Arabidopsis plants, HFB9A protein induced phosphorylation of AtMAPK3/6, suggesting that it functions as a microbe-associated molecular pattern.

plant biology↗

bioRxiv2019

Persistence and plasticity of T follicular memory cells

CD4 memory T cells play an important role in protective immunity and are a key target in vaccine development. Many studies have focused on T central memory (TCM) cells, while the existence and functional significance of T follicular helper (TFH) memory cells is controversial. Here we show that TFH memory cells are highly susceptible to NAD induced cell death (NICD) during isolation from tissues, leading to their under-representation in prior studies. NICD blockade reveals the persistence of abundant TFH memory cells, with high expression of hallmark TFH markers, that persist to at least 400 days after infection, by which time TCM cells are no longer found. Using single cell RNA-seq we demonstrate that TFH memory cells are transcriptionally distinct from TCM cells, maintain stemness and self-renewal gene expression, and, in contrast to TCM cells, are multipotent following recall. Surprisingly, TFH memory cells concurrently express a distinct glycolytic signature similar to trained immune cells, including elevated expression of mTOR, HIF-1 and cAMP regulated genes. Late disruption of glycolysis/ICOS signaling leads to TFH memory cell depletion concomitant with decreased splenic plasma cells and circulating antibody titers, demonstrating both unique homeostatic regulation of memory TFH and their sustained function during the memory phase of the immune response. These results highlight the metabolic heterogeneity underlying distinct memory T cell subsets and establish TFH memory cells as an attractive target for the induction of long-lived adaptive immunity.\n\nHIGHLIGHTSO_LICell death during isolation from the tissue prevents the full recovery of TFH memory cells\nC_LIO_LITFH memory cells are transcriptionally distinct from TCM cells and maintain a broader recall capacity\nC_LIO_LITFH memory cells are maintained in the absence of antigen but require ICOS signaling and glycolysis\nC_LIO_LITFH memory cells support late phase antibody production by splenic plasma cells\nC_LI

immunology↗