title: Deletion of regulatory T cells supports the development of intestinal ischemia-reperfusion injuries.
abstract: BACKGROUND
  Ischemia-reperfusion injury (IRI) of the intestine is associated with high morbidity and mortality in surgical and trauma patients. T cells participate in the pathogenesis of intestinal IRI, and T-cell depletion has been shown to inhibit inflammatory responses and diminish intestinal damage. However, the mechanism by which T cells contribute to intestinal IRI is not completely understood. Regulatory T cells (Tregs) are a specific subset of T cells that suppress immune responses and protect against tissue injuries. We hypothesized that Tregs might be involved in intestinal IRI.
  
  
  METHODS
  We subjected C57/Bl6 mice to 30 min of ischemia by clamping the superior mesenteric artery followed by reperfusion. Animals were pretreated with the anti-CD25 monoclonal antibody or adoptive transfer of Tregs before induction of IRI. The number of inflammatory cells, the level of inflammatory factors, and intestinal permeability were assessed.
  
  
  RESULTS
  Partial depletion of Tregs with an anti-CD25 monoclonal antibody potentiated intestinal permeability induced by IRI. The Treg-depleted mice showed more neutrophils and CD4(+) T cells. In addition, depletion of Tregs led to enhanced secretion of tumor necrosis factor-α, interferon-gamma, and interleukin (IL)-4 and reduced levels of IL-10. Furthermore, we performed adoptive transfer of Tregs and found that transfer of Tregs significantly inhibited the ischemia-reperfusion-induced increase in intestinal permeability.
  
  
  CONCLUSIONS
  Our study indicated that Tregs participate in intestinal inflammatory responses induced by IRI and that targeting Tregs could be a novel therapeutic approach to intestinal IRI.
authors.affiliation: Department of Burns and Cutaneous Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shannxi, People's Republic of China.
authors.forename: Xuekang
authors.initials: X
authors.lastname: Yang
authors.forename: Hua
authors.initials: H
authors.lastname: Bai
authors.forename: Yunchuan
authors.initials: Y
authors.lastname: Wang
authors.forename: Jun
authors.initials: J
authors.lastname: Li
authors.forename: Qin
authors.initials: Q
authors.lastname: Zhou
authors.forename: Weixia
authors.initials: W
authors.lastname: Cai
authors.forename: Juntao
authors.initials: J
authors.lastname: Han
authors.forename: Xiongxiang
authors.initials: X
authors.lastname: Zhu
authors.forename: Maolong
authors.initials: M
authors.lastname: Dong
authors.forename: Dahai
authors.initials: D
authors.lastname: Hu
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D002452:Cell Count; D007249:Inflammation / Q000473:pathology* / Q000503:physiopathology*; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D053645:Interleukin-2 Receptor alpha Subunit / Q000187:drug effects / Q000276:immunology; D015847:Interleukin-4 / Q000378:metabolism; D007422:Intestines / Q000098:blood supply* / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D053645:Interleukin-2 Receptor alpha Subunit; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma
keywords: Inflammation; Ischemia-reperfusion; Regulatory T cells; Small intestine