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Herter, Jan M.

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Herter

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Jan M.

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Herter, Jan M.

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2014 - 20152

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Author's Publications: search.filters.isAuthorOfPublication.b21d0367-e218-4477-8ebb-333892f3ae9f

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    Image-guided radiotherapy platform using single nodule conditional lung cancer mouse models
    (2014) Herter-Sprie, Grit S.; Korideck, Houari; Christensen, Camilla L.; Herter, Jan M.; Rhee, Kevin; Berbeco, Ross; Bennett, David G.; Akbay, Esra A.; Kozono, David; Mak, Raymond; Makrigiorgos, Gerassimos; Kimmelman, Alec C.; Wong, Kwok-Kin
    Close resemblance of murine and human trials is essential to achieve the best predictive value of animal-based translational cancer research. Kras-driven genetically engineered mouse models of non-small cell lung cancer faithfully predict the response of human lung cancers to systemic chemotherapy. Due to development of multifocal disease, however, these models have not been usable in studies of outcomes following focal radiotherapy (RT). We report the development of a preclinical platform to deliver state-of-the-art image-guided RT in these models. Presence of a single tumour as usually diagnosed in patients is modelled by confined injection of adenoviral Cre recombinase. Furthermore, three-dimensional conformal planning and state-of-the-art image-guided dose delivery are performed as in humans. We evaluate treatment efficacies of two different radiation regimens and find that Kras-driven tumours can temporarily be stabilized upon RT, whereas additional loss of either Lkb1 or p53 renders these lesions less responsive to RT.
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    AKAP9 regulates activation-induced retention of T lymphocytes at sites of inflammation
    (Nature Publishing Group, 2015) Herter, Jan M.; Grabie, Nir; Cullere, Xavier; Azcutia, Veronica; Rosetti, Florencia; Bennett, Paul; Herter-Sprie, Grit S.; Elyaman, Wassim; Luscinskas, Francis; Lichtman, Andrew; Mayadas, Tanya
    The mechanisms driving T cell homing to lymph nodes and migration to tissue are well described but little is known about factors that affect T cell egress from tissues. Here, we generate mice with a T cell-specific deletion of the scaffold protein A kinase anchoring protein 9 (AKAP9) and use models of inflammatory disease to demonstrate that AKAP9 is dispensable for T cell priming and migration into tissues and lymph nodes, but is required for T cell retention in tissues. AKAP9 deficiency results in increased T cell egress to draining lymph nodes, which is associated with impaired T cell re-activation in tissues and protection from organ damage. AKAP9-deficient T cells exhibit reduced microtubule-dependent recycling of TCRs back to the cell surface and this affects antigen-dependent activation, primarily by non-classical antigen-presenting cells. Thus, AKAP9-dependent TCR trafficking drives efficient T cell re-activation and extends their retention at sites of inflammation with implications for disease pathogenesis.