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
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)

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