Biology subjects

Laliberte, A.

Publications and source records attributed to Laliberte, A..

3 recordsLinked to original sources

bioRxiv2025

Poly-L-Ornithine Coated Plant Scaffolds Support Motor Recovery in Rats after Traumatic Spinal Cord Injury

Spinal cord injury (SCI) is a debilitating neurological condition with far-reaching consequences for patients, including loss of motor function and significant limitations to quality of life. Implantable biomaterials have emerged as a therapeutic strategy to modulate the SCI microenvironment and facilitate regeneration of axons. In this study, plant-derived lignocellulosic scaffolds coated with poly-L-ornithine (PLO) are shown to support locomotor recovery and neural tissue repair in a rat model of spinal cord injury. Upon complete transection of the spinal cord, animals were implanted with a plant-derived scaffold coated in poly-L-ornithine, a positively charged amino acid chain that is known to promote neural stem cell differentiation into neurons and enhance myelin regeneration. Recovery of motor function was evaluated by the Basso, Beattie and Bresnahan (BBB) locomotor scale as well as the Karolinska Institutet Swim Assessment Tool (KSAT). Retrograde tracing of ascending sensory tracts revealed enhanced regeneration in animals that received the PLO-coated scaffold. Numerous {beta}-III tubulin and neurofilament 200 positive fibers may indicate axonal sprouting within the lignocellulosic scaffold and LFB staining highlights myelination around the PLO-coated scaffold. These results demonstrate the potential of plant-based biomaterials in a rat model of acute spinal cord injury and highlight their enhancement after PLO functionalization.

bioengineering↗

bioRxiv2023

Traitor-virus-guided discovery of novel antiviral factors

Complex pathogen-host interactions govern the outcome of viral exposures but remain poorly understood because current methods to elucidate antiviral mechanisms are prone to artefacts and lack sensitivity. Here, we developed a virus-guided technology platform where the pathogen itself reveals its cellular opponents. To accomplish this, we engineered replication-competent HIV-1 expressing sgRNAs targeting potential antiviral genes in Cas9-expressing CD4+ T cells. Simultaneous analysis of HIV-1 constructs targeting >500 candidate genes revealed that sgRNAs against GRN, CIITA, EHMT2, CEACAM3, CC2D1B, RHOA and HMOX1 are strongly enriched over several rounds of replication. Overexpression and knock-out studies confirmed the antiretroviral activity of most factors but failed for some. Finally, we show that lack of the accessory nef gene increased enrichment of sgRNAs targeting SERINC5 and IFI16 demonstrating that this method allows identification of targets of accessory proteins. The versatile and effective HIV-guided CRISPR technology offers numerous possibilities for clarification of virus-host interactions and innate defense mechanisms.

microbiology↗

bioRxiv2019

ILT7 activation and plasmacytoid dendritic cell response are governed by BST2 determinants that are structurally-distinct

The interaction of the human pDC receptor ILT7 with its ligand, BST2, significantly regulates pDCs TLR-induced innate immune responses. This interaction has critical biological consequences, yet, its structural requirements are not fully characterized. The BST2 ectodomain can be divided in structurally and functionally distinct regions; while the coiled-coil region contains a newly-defined ILT7 binding surface, the N-terminal region appears to negatively modulate ILT7 activation. A stable BST2 homodimer binds to ILT7 but post-binding events associated to the unique BST2 coiled-coil plasticity are required to trigger receptor signaling. Hence, BST2 with an unstable or with a rigid coiled-coil fails to activate ILT7, whereas mutations in the N-terminal region enhance activation. Importantly, the biological relevance of these newly defined domains of BST2 is underscored by the identification of mutations with opposed potential to activate ILT7, which are selected under pathological malignant conditions.

immunology↗