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20231226071938.0 |
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231226s2023 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2023.109647
|2 doi
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|a pubmed24n1190.xml
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|a (DE-627)NLM357137876
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|a (NLM)37211291
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|a (PII)S1521-6616(23)00146-8
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Chen, Yuqi
|e verfasserin
|4 aut
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| 245 |
1 |
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|a T cell specific deletion of IRF4 with Ox40-Cre impairs effector and memory T cell responses in heart transplantation
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|c 2023
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 22.06.2023
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|a Date Revised 22.06.2023
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2023. Published by Elsevier Inc.
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|a BACKGROUND: IRF4 is the pioneer factor for effector T cell maturation. Here we investigated the function of IRF4 in maintaining OX40-related T cell responses following alloantigen activation in a mouse heart transplantation model
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|a METHODS: Irf4flox/flox mice were bred with Ox40cre/+ mice to generate Irf4flox/floxOx40cre/+ mice. Wild type C57BL/6, Irf4flox/floxOx40cre/+ mice were transplanted with BALB/c heart allografts, with or without BALB/c skin-sensitization. CD4+ TEa T cells co-transfer experiments and flow cytometric analysis were conducted to investigate the amount of CD4+ T cells and the percentage of the T effector subset
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| 520 |
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|a RESULTS: Irf4flox/floxOx40cre/+ and Irf4flox/floxOx40cre/+ TEa mice were constructed successfully. IRF4 ablation in activated OX40-mediated alloantigen specific CD4+ TEa T cells reduced effector T cell differentiation (CD44hiCD62Llo, Ki67, IFN-γ), which caused long-term allograft survival (> 100 d) in the chronic rejection model. In the donor skin-sensitized heart transplantation model, the formation and function of alloantigen-specific memory CD4+ TEa cells were also impaired in Irf4flox/floxOx40cre/+ mice. Additionally, deletion of IRF4 after T cell activation in Irf4flox/floxOx40cre/+ mice reduced T cell reactivation in vitro
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|a CONCLUSIONS: IRF4 ablation after OX40-related T cell activation could reduce effector and memory T cell formation and inhibit their function in response to alloantigen stimulation. These findings could have significant implications in targeting activated T cells to induce transplant tolerance
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Heart transplantation
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| 650 |
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|a T cell differentiation
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|a Transplant tolerance
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| 650 |
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|a Transplantantion immunity
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| 650 |
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|a Cre recombinase
|2 NLM
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| 650 |
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|a EC 2.7.7.-
|2 NLM
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| 650 |
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|a Isoantigens
|2 NLM
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| 650 |
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|a interferon regulatory factor-4
|2 NLM
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| 700 |
1 |
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|a Liu, Zongtao
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Liu, Fayuan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Xu, Li
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Li, Geng
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Qiao, Weihua
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Yixuan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Dong, Nianguo
|e verfasserin
|4 aut
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| 773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 252(2023) vom: 30. Juli, Seite 109647
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:252
|g year:2023
|g day:30
|g month:07
|g pages:109647
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2023.109647
|3 Volltext
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