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http://doi.org/10.25358/openscience-7766
Autoren: | Mufazalov, Ilgiz A. Regen, Tommy Schelmbauer, Carsten Kuschmann, Janina Muratova, Alisa M. Nikolaev, Alexei Müller, Werner Pinteaux, Emmanuel Waisman, Ari |
Titel: | Generation of a novel T cell specific interleukin-1 receptor type 1 conditional knock out mouse reveals intrinsic defects in survival, expansion and cytokine production of CD4 T cells |
Online-Publikationsdatum: | 15-Sep-2022 |
Erscheinungsdatum: | 2016 |
Sprache des Dokuments: | Englisch |
Zusammenfassung/Abstract: | Interleukin-1 (IL-1) plays a crucial role in numerous inflammatory diseases via action on its only known signaling IL-1 receptor type 1 (IL-1R1). To investigate the role of IL-1 signaling in selected cell types, we generated a new mouse strain in which exon 5 of the Il1r1 gene is flanked by loxP sites. Crossing of these mice with CD4-Cre transgenic mice resulted in IL-1R1 loss of function specifically in T cells. These mice, termed IL-1R1ΔT, displayed normal development under steady state conditions. Importantly, isolated CD4 positive T cells retained their capacity to differentiate toward Th1 or Th17 cell lineages in vitro, and strongly proliferated in cultures supplemented with either anti-CD3/CD28 or Concanavalin A, but, as predicted, were completely unresponsive to IL-1β administration. Furthermore, IL-1R1ΔT mice were protected from gut inflammation in the anti-CD3 treatment model, due to dramatically reduced frequencies and absolute numbers of IL-17A and interferon (IFN)-γ producing cells. Taken together, our data shows the necessity of intact IL-1 signaling for survival and expansion of CD4 T cells that were developed in an otherwise IL-1 sufficient environment. |
DDC-Sachgruppe: | 610 Medizin 610 Medical sciences |
Veröffentlichende Institution: | Johannes Gutenberg-Universität Mainz |
Organisationseinheit: | FB 04 Medizin |
Veröffentlichungsort: | Mainz |
ROR: | https://ror.org/023b0x485 |
DOI: | http://doi.org/10.25358/openscience-7766 |
Version: | Published version |
Publikationstyp: | Zeitschriftenaufsatz |
Nutzungsrechte: | CC BY |
Informationen zu den Nutzungsrechten: | https://creativecommons.org/licenses/by/4.0/ |
Zeitschrift: | PLoS one 11 8 |
Seitenzahl oder Artikelnummer: | e0161505 |
Verlag: | PLoS |
Verlagsort: | Lawrence, Kan. |
Erscheinungsdatum: | 2016 |
ISSN: | 1932-6203 |
URL der Originalveröffentlichung: | http://dx.doi.org/10.1371/journal.pone.0161505 |
DOI der Originalveröffentlichung: | 10.1371/journal.pone.0161505 |
Enthalten in den Sammlungen: | DFG-OA-Publizieren (2012 - 2017) |
Dateien zu dieser Ressource:
Datei | Beschreibung | Größe | Format | ||
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generation_of_a_novel_t_cell_-20220913200649971.pdf | 3.45 MB | Adobe PDF | Öffnen/Anzeigen |