Deletion of Foxp3+ regulatory T cells in genetically targeted mice supports development of intestinal inflammation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-07-31

AUTHORS

Franziska Boehm, Maria Martin, Rebecca Kesselring, Gabriela Schiechl, Edward K Geissler, Hans-Jürgen Schlitt, Stefan Fichtner-Feigl

ABSTRACT

BACKGROUND: Mice lacking Foxp3+ regulatory T (Treg) cells develop severe tissue inflammation in lung, skin, and liver with premature death, whereas the intestine remains uninflamed. This study aims to demonstrate the importance of Foxp3+ Treg for the activation of T cells and the development of intestinal inflammation. METHODS: Foxp3-GFP-DTR (human diphtheria toxin receptor) C57BL/6 mice allow elimination of Foxp3+ Treg by treatment with Dx (diphtheria toxin). The influence of Foxp3+ Treg on intestinal inflammation was tested using the CD4+ T-cell transfer colitis model in Rag-/- C57BL/6 mice and the acute DSS-colitis model. RESULTS: Continuous depletion of Foxp3+ Treg in Foxp3-GFP-DTR mice led to dramatic weight loss and death of mice by day 28. After 10 days of depletion of Foxp3+ Treg, isolated CD4+ T-cells were activated and produced extensive amounts of IFN-γ, IL-13, and IL-17A. Transfer of total CD4+ T-cells isolated from Foxp3-GFP-DTR mice did not result in any changes of intestinal homeostasis in Rag-/- C57BL/6 mice. However, administration of DTx between days 14 and 18 after T-cell reconstitution, lead to elimination of Foxp3+ Treg and to immediate weight loss due to intestinal inflammation. This pro-inflammatory effect of Foxp3+ Treg depletion consecutively increased inflammatory cytokine production. Further, the depletion of Foxp3+ Treg from Foxp3-GFP-DTR mice increased the severity of acute dSS-colitis accompanied by 80% lethality of Treg-depleted mice. CD4+ effector T-cells from Foxp3+ Treg-depleted mice produced significantly more pro-inflammatory cytokines. CONCLUSION: Intermittent depletion of Foxp3+ Treg aggravates intestinal inflammatory responses demonstrating the importance of Foxp3+ Treg for the balance at the mucosal surface of the intestine. More... »

PAGES

97-97

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1471-230x-12-97

DOI

http://dx.doi.org/10.1186/1471-230x-12-97

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1037790647

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22849659


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70 changes
71 colitis model
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73 cytokine production
74 cytokines
75 day 14
76 day 28
77 days
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79 death
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81 deletion
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83 depletion of Foxp3
84 development
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86 effect
87 effector T
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90 extensive amount
91 homeostasis
92 importance
93 importance of Foxp3
94 inflammation
95 inflammatory cytokine production
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97 influence
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100 intestinal inflammation
101 intestinal inflammatory response
102 intestine
103 lead
104 lethality
105 lethality of Treg
106 liver
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108 lung
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111 mucosal surfaces
112 premature death
113 pro-inflammatory cytokines
114 pro-inflammatory effects
115 production
116 reconstitution
117 response
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119 severity
120 skin
121 study
122 surface
123 tissue inflammation
124 total CD4
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