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Alexandre J. Potocnik

Researcher at University of Edinburgh

Publications -  45
Citations -  4877

Alexandre J. Potocnik is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Antigen & T cell. The author has an hindex of 24, co-authored 45 publications receiving 4295 citations. Previous affiliations of Alexandre J. Potocnik include Max Planck Society & National Institute for Medical Research.

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Fate mapping of IL-17-producing T cells in inflammatory responses

TL;DR: A reporter mouse strain designed to map the fate of cells that have activated interleukin 17A (IL-17A) allows the actual functional fate of effector T cells to be related to TH17 developmental origin regardless of IL-17 expression.
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Transgenic mice with hematopoietic and lymphoid specific expression of Cre.

TL;DR: Mouse lines expressing Cre recombinase in hematopoietic tissues using the vav regulatory elements, or in lymphoid cells using the hCD2 promoter and locus control region (LCR) are generated, which will be useful in generating tissue‐specific gene deletions within all the cells of hematoplastic or lymphoid tissues.
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Fetal and Adult Hematopoietic Stem Cells Require β1 Integrin Function for Colonizing Fetal Liver, Spleen, and Bone Marrow

TL;DR: It is shown that beta1 integrin-deficient HSCs from the para-aortic splanchnopleura and the fetal blood had hematolymphoid differentiation potential in vitro and in fetal organ cultures but were unable to seed fetal and adult hematopoietic tissues.
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Feedback control of AHR signalling regulates intestinal immunity.

TL;DR: The data indicate that intestinal epithelial cells serve as gatekeepers for the supply of AHR ligands to the host and emphasize the importance of feedback control in modulating AHR pathway activation.
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Glial cells in the mouse enteric nervous system can undergo neurogenesis in response to injury

TL;DR: It is demonstrated that mouse neural crest cells marked by SRY box-containing gene 10 (Sox10) generate the neuronal and glial lineages of enteric ganglia, and enteric glia maintain limited neurogenic potential, which can be activated by tissue dissociation or injury.