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| Status |
Public on Oct 13, 2020 |
| Title |
Kidney GATA3+ regulatory T cells play roles in the convalescence stage after antibody-mediated renal injury |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by array
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| Summary |
FoxP3+ regulatory T cells (Tregs) play crucial roles in peripheral immune tolerance. In addition, Tregs that reside or accumulate in nonlymphoid tissues, called tissue Tregs, exhibit tissue-specific functions and contribute to the maintenance of tissue homeostasis and repair. In an experimental mouse model of crescentic glomerulonephritis induced by an anti-glomerular basement membrane antibody, Tregs started to accumulate in the kidney on day 10 of disease onset and remained at high levels (~30–35% of CD4+ T cells) during the late stage (days 21–90), which correlated with stable disease control. Treg depletion on day 21 resulted in the relapse of renal dysfunction and an increase in Th1 cells, suggesting that Tregs are essential for disease control during the convalescence stage. The Tregs that accumulated in the kidney showed tissue Treg phenotypes, including high expression of GATA3, ST2 (the IL33 receptor subunit), amphiregulin (Areg), and PPARγ. Although T-bet+ Tregs and RORγt+ Tregs were observed in the kidney, GATA3+ Tregs were predominant during the convalescence stage, and a PPARγ agonist enhanced the accumulation of GATA3+ Tregs in the kidney. To understand the function of specific genes in kidney Tregs, we developed a novel T cell transfer system to T cell-deficient mice. This experiment demonstrates that ST2, Areg, and CCR4 in Tregs play important roles in the accumulation of GATA3+ Tregs in the kidney and in the amelioration of renal injury. Our data suggest that GATA3 is important for the recruitment of Tregs into the kidney, which is necessary for convalescence after renal tissue destruction.
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| Overall design |
Tregs (CD45+CD3e+CD4+FoxP3-hCD2+ T cells) from renal tissue were isolated on day 28 after cGN induction. Total RNA was isolated using a TRIzol LS reagent (Invitrogen).Disease severity was depended on variation among lots of anti-GBM antibodies in this experiments. To improve the quality of this analysis, we used the two lots of anti-GBM antibodies, M and I.
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| Contributor(s) |
Sakai R, Ito M |
| Citation missing |
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| Submission date |
Oct 12, 2020 |
| Last update date |
Oct 22, 2020 |
| Contact name |
Minako Ito |
| E-mail(s) |
minakoito@bioreg.kyushu-u.ac.jp
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| Organization name |
Kyushu University
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| Street address |
3-1-1 Maidashi, Higashi-ku
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| City |
Fukuoka |
| ZIP/Postal code |
812-8582 |
| Country |
Japan |
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| Platforms (1) |
| GPL21163 |
Agilent-074809 SurePrint G3 Mouse GE v2 8x60K Microarray [Probe Name version] |
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| Samples (2) |
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| Relations |
| BioProject |
PRJNA668850 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE159420_RAW.tar |
17.7 Mb |
(http)(custom) |
TAR (of TXT) |
| Processed data included within Sample table |
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