Please use this identifier to cite or link to this item:
http://doi.org/10.25358/openscience-7766
Authors: | Mufazalov, Ilgiz A. Regen, Tommy Schelmbauer, Carsten Kuschmann, Janina Muratova, Alisa M. Nikolaev, Alexei Müller, Werner Pinteaux, Emmanuel Waisman, Ari |
Title: | 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 publication date: | 15-Sep-2022 |
Year of first publication: | 2016 |
Language: | english |
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: | 610 Medizin 610 Medical sciences |
Institution: | Johannes Gutenberg-Universität Mainz |
Department: | FB 04 Medizin |
Place: | Mainz |
ROR: | https://ror.org/023b0x485 |
DOI: | http://doi.org/10.25358/openscience-7766 |
Version: | Published version |
Publication type: | Zeitschriftenaufsatz |
License: | CC BY |
Information on rights of use: | https://creativecommons.org/licenses/by/4.0/ |
Journal: | PLoS one 11 8 |
Pages or article number: | e0161505 |
Publisher: | PLoS |
Publisher place: | Lawrence, Kan. |
Issue date: | 2016 |
ISSN: | 1932-6203 |
Publisher URL: | http://dx.doi.org/10.1371/journal.pone.0161505 |
Publisher DOI: | 10.1371/journal.pone.0161505 |
Appears in collections: | DFG-OA-Publizieren (2012 - 2017) |
Files in This Item:
File | Description | Size | Format | ||
---|---|---|---|---|---|
generation_of_a_novel_t_cell_-20220913200649971.pdf | 3.45 MB | Adobe PDF | View/Open |