title: [Tumor necrosis factor-α-induced protein 8 like-2 promotes apoptosis of CD4+T lymphocytes in mice with severe burn injury].
abstract: OBJECTIVE
  To investigate the effect of tumor necrosis factor-α-induced protein 8 like-2 (TIPE2) on apoptosis of CD4+T lymphocytes in a murine model of severe burn injury.
  
  
  METHODS
  A total of 140 male mice were randomly allocated into 6 groups. Small RNA interference technique was used to construct a siTIPE2-overexpressing lentivirus, and severe burn injury models were established in the mice. CD4+T cells were purified from spleen of the mice, and the expressions of TIPE2, Smad2/Smad3, P-Smad2/P-Smad3 and Bcl-2/Bimprotein in CD4+Tregs were detected. The changes in mitochondrial membrane potential and cytochrome C in CD4+T cells were detected, and the activities of caspase-3, caspase-8, and caspase-9 were analyzed.
  
  
  RESULTS
  Down-regulation of TIPE2 promoted the apoptosis of CD4+T lymphocytes in siTIPE2-burn group, in which the protein expressions of P-smad2/P-Smad3 decreased, Bcl-2 expression increased and Bim expression decreased significantly as compared with the other groups (P<0.01 or 0.05). The mitochondrial membrane potential and cytochrome C expression in CD4+T cells were down-regulated in siTIPE2-burn group (P<0.05) with a lowered caspase-3 activity compared with TIPE2-burn group (P<0.01) and decreased caspase-8 and caspase-9 compared with the other groups (P<0.05). The apoptosis rate was the highest in TIPE2-burn group, whose Smad2/Smad3 was higher than that in the sham group (P<0.05) and the expression of P-smad2/P-Smad3 significantly increased compared with the other groups (P<0.05). In TIPE2-burn group, the mitochondrial membrane potential in CD4+T cells was decreased (P<0.01), the expression of cytochrome C increased markedly (P<0.01), and the activities of caspase-3, caspase-8, and caspase-9 were all obviously higher than those in the other groups (P<0.05).
  
  
  CONCLUSIONS
  As an important immunoregulatory molecule, TIPE2 can promote the apoptosis of CD4+T lymphocyte in mice with sever burn injury.
authors: 1Emergency Department, Chinese PLA General Hospital, Beijing 100853, China; 2Department of Critical Care Medicine, General Hospital of Jinan Command, Jinan 250031, China. E-mail: huanghe_hh@126.com.
authors: He
authors: H
authors: Huang
authors: Zhao-Tao
authors: ZT
authors: Tian
authors: Yong-Ming
authors: YM
authors: Yao
authors: Tan-Shi
authors: TS
authors: Li
mesh_terms: D000818:Animals; D017209:Apoptosis; D002056:Burns / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology*; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D015536:Down-Regulation; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism*; D008297:Male; D051379:Mice; D051899:Smad2 Protein / Q000378:metabolism; D051900:Smad3 Protein / Q000378:metabolism; D013154:Spleen
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D051899:Smad2 Protein; C497783:Smad2 protein, mouse; D051900:Smad3 Protein; C497791:Smad3 protein, mouse; C529002:TIPE2 protein, mouse; C505409:Casp3 protein, mouse; C505526:Casp8 protein, mouse; C506434:Casp9 protein, mouse; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9