scholarly journals IKK  is involved in kidney recovery and regeneration of acute ischemia/reperfusion injury in mice through IL10-producing regulatory T cells

2015 ◽  
Vol 8 (7) ◽  
pp. 733-742 ◽  
Author(s):  
X. Wan ◽  
L.-J. Hou ◽  
L.-Y. Zhang ◽  
W.-J. Huang ◽  
L. Liu ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acute Ischemia

scholarly journals Netrin-1 reduces lung ischemia-reperfusion injury by increasing the proportion of regulatory T cells

2020 ◽  
Vol 48 (6) ◽  
pp. 030006052092641
Author(s):  
Zhili Chen ◽  
Yuxi Chen ◽  
Jue Zhou ◽  
Yong Li ◽  
Changyao Gong ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cells ◽  
Regulatory T Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Axonal Guidance ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Treg Depletion

Objective Inflammation is the primary mechanism of lung ischemia-reperfusion injury (LIRI) and neurologic factors can regulate inflammatory immune responses. Netrin-1 is an axonal guidance molecule, but whether Netrin-1 plays a role in LIRI remains unclear. Methods A mouse model of LIRI was established. Immunohistochemistry was used to detect expression of Netrin-1 and to enumerate macrophages and T cells in lung tissue. The proportion of regulatory T cells (Tregs) was assessed by flow cytometry. Levels of apoptosis were assessed by terminal deoxynucleotidyl transferase dUTP nick end staining. Results Numbers of macrophages and T cells in the lung tissues of mice with LIRI were elevated, while expression of netrin-1 was significantly decreased. Flow cytometry showed that the proportion of Tregs in mice with LIRI was significantly decreased. The proportion of Tregs among lymphocytes was positively correlated with netrin-1 expression. In vitro experiments showed that netrin-1 promoted an increase in Treg proportion through the A2b receptor. Animal experiments showed that netrin-1 could inhibit apoptosis and reduce T cell and macrophage infiltration by increasing the proportion of Tregs, ultimately reducing LIRI. Treg depletion using an anti-CD25 monoclonal antibody blocked the effects of netrin-1. Conclusion Netrin-1 reduced LIRI by increasing the proportion of Tregs.

Regulatory T cells contribute to rosuvastatin-induced cardioprotection against ischemia-reperfusion injury

2013 ◽  
Vol 24 (4) ◽  
pp. 334-341 ◽  
Author(s):  
Dan Ke ◽  
Jun Fang ◽  
Lin Fan ◽  
Zhaoyang Chen ◽  
Lianglong Chen
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

scholarly journals Regulatory T Cells Suppress Innate Immunity in Kidney Ischemia-Reperfusion Injury

2009 ◽  
Vol 20 (8) ◽  
pp. 1744-1753 ◽  
Author(s):  
Gilbert R. Kinsey ◽  
Rahul Sharma ◽  
Liping Huang ◽  
Li Li ◽  
Amy L. Vergis ◽  
...  
Keyword(s):  
Innate Immunity ◽  
T Cells ◽  
Regulatory T Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Ischemia

scholarly journals MP29-10 PROTECTIVE EFFECTS OF REGULATORY T CELLS IN RENAL ISCHEMIA/REPERFUSION INJURY IN MICE

2016 ◽  
Vol 195 (4S) ◽  
Author(s):  
Ryohei Yamamoto ◽  
Mitsuru Saito ◽  
Hiroshi Tsuruta ◽  
Atsushi Maeno ◽  
Takamitsu Inoue ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Protective Effects ◽  
Renal Ischemia Reperfusion Injury

scholarly journals Protective Effect of CXCR3+CD4+CD25+Foxp3+Regulatory T Cells in Renal Ischemia-Reperfusion Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Cao Jun ◽  
Li Qingshu ◽  
Wei Ke ◽  
Li Ping ◽  
Dong Jun ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Tubular Necrosis ◽  
Renal Ischemia Reperfusion Injury ◽  
Histology Score

Regulatory T cells (Tregs) suppress excessive immune responses and are potential therapeutic targets in autoimmune disease and organ transplantation rejection. However, their role in renal ischemia-reperfusion injury (IRI) is unclear. Levels of Tregs and expression of CXCR3 in Tregs were analyzed to investigate their function in the early phase of renal IRI. Mice were randomly divided into Sham, IRI, and anti-CD25 (PC61) + IRI groups. The PC61 + IRI group was established by i.p. injection of PC61 monoclonal antibody (mAb) to deplete Tregs before renal ischemia. CD4+CD25+Foxp3+Tregs and CXCR3 on Tregs were analyzed by flow cytometry. Blood urea nitrogen (BUN), serum creatinine (Scr) levels, and tubular necrosis scores, all measures of kidney injury, were greater in the IRI group than in the Sham group. Numbers of Tregs were increased at 72 h after reperfusion in kidney. PC61 mAb preconditioning decreased the numbers of Tregs and aggravated kidney injury. There was no expression of CXCR3 on Tregs in normal kidney, while it expanded at 72 h after reperfusion and inversely correlated with BUN, Scr, and kidney histology score. This indicated that recruitment of Tregs into the kidney was related to the recovery of renal function after IRI and CXCR3 might be involved in the migration of Tregs.

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