Technology/Services
- T cell Tracker
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- The inappropriate activation of CD4+ T cells is a central component to many chronic immune-pathologies, including autoimmune and allergic disease. We have established in vitro assays to best mimic the in vivo activation of T cells under a range of different inflammatory contexts (Th1, Th2, Th17 etc).
Our T cell Tracker technology allows us to specifically follow the fate and function of those same T cells in response to antigen-mediated inflammatory conditions in vivo. We can also follow T cells that are programmed to have particular inflammatory functions (as above).
This platform provides:-- Moderate throughput in vitro assays giving rapid high-value mode-of-action data for lead compound selection.
- In life validation of on target effects under a range of pro-inflammatory T cell functions.
- The inappropriate activation of CD4+ T cells is a central component to many chronic immune-pathologies, including autoimmune and allergic disease. We have established in vitro assays to best mimic the in vivo activation of T cells under a range of different inflammatory contexts (Th1, Th2, Th17 etc).
- MBP-Tracker
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- Experimental autoimmune encephalomyelitis (EAE) is induced by immunization with autoantigens from CNS myelin. CNS pathology is driven by the actions of CD4+ T cells activated by the autoantigen. The standard EAE models provide efficacy data, but supportive ex vivo assays are limited.
Our MBP-Tracker technology allows us to specifically follow those T cells that drive pathology, quantify them in different organs (including the CNS) and to measure the activation of a range of key disease-associated functions within these T cells. We therefore provide high-value mode-of-action studies to complement efficacy data.
We have established moderate throughput in vitro assays to best mimic the in vivo activation of pathogenic T cells. These allow us to study the same pathogenic T cells in vitro to obtain the best indication of the pathways targeted by your compounds, allowing you to progress more efficiently to in-life studies.
Contact us for more information.
- Experimental autoimmune encephalomyelitis (EAE) is induced by immunization with autoantigens from CNS myelin. CNS pathology is driven by the actions of CD4+ T cells activated by the autoantigen. The standard EAE models provide efficacy data, but supportive ex vivo assays are limited.
- OPC Cultures and Remyelination
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- Remyelination of nerves occurs in MS, but it is inefficient and becomes less so as the disease progresses. Remyelination not only restores proper nerve conduction, but it also protects axons from degeneration. Improving remyelination efficiency is therefore likely to reduce disease progression in MS. For remyelination to occur, oligodendrocyte precursor cells (OPC) around lesions must survive and proliferate, differentiate into myelinating oligodendrocytes and then carry out remyelination. In-life models of focal demyelination are technically demanding and expensive.
Aquila BioMedical has developed a suite of in-vitro assay systems, with automated, quantitative image analyses that allow moderate throughput screening for more efficient compound selection.
- OPC cultures Toxicity testing allows the rate of OPC proliferation and cell death in the presence of your compound to be determined. Immunohistochemical assays using markers for immature and mature oligodendrocytes allow the quantification of your compound's ability to stimulate OPC differentiation into oligodendrocytes.
- Remyelination in CNS slice cultures Rodent CNS slice cultures show remyelination following toxin-induced demyelination. The ability of your compound to speed remyelination is assessed using immunohistochemistry. Analysis is automated, allowing moderate-throughput and high-content screening. The predictive power of this assay has been validated in life.
- Remyelination of nerves occurs in MS, but it is inefficient and becomes less so as the disease progresses. Remyelination not only restores proper nerve conduction, but it also protects axons from degeneration. Improving remyelination efficiency is therefore likely to reduce disease progression in MS. For remyelination to occur, oligodendrocyte precursor cells (OPC) around lesions must survive and proliferate, differentiate into myelinating oligodendrocytes and then carry out remyelination. In-life models of focal demyelination are technically demanding and expensive.
- Immunoassays
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- T cell activation assays:
- Proliferation (thymidine incorporation, CFSE-dilution by FACS).
- Cytokine production.
- Activation markers (FACS).
- Gene expression (qPCR).
- Innate immune cell activation assays (including dendritic cell functional assays).
- Antigen presentation assays.
- Analysis of cytokines, chemokines and inflammatory mediators from culture supernatants or biological fluids (ELISA and multiplex bead arrays).
- Antibody (isotype) quantitation (ELISA).
- Immunohistochemistry / Immunofluorescence / confocal imaging.
- Multi-parameter Flow cytometry (cell surface and intracellular staining).
- FACS-sorting for downstream analysis (including gene expression).
- T cell activation assays: