title: Micro-inflammation characterized by disturbed Treg/Teff balance with increasing sIL-2R in patients with type 2 diabetes.
abstract: OBJECTIVE
  Type 2 diabetes mellitus (T2DM) has been gradually considered as a micro- inflammatory disease. To explore the significance of peripheral CD4(+) regulatory T cells and CD4(+) effector T cells in T2DM, we analyzed inflammation, humoral and cellular immune state in patients with T2DM.
  
  
  METHODS
  118 patients with T2DM without complications and 116 healthy volunteers were included. Serum C-reactive protein (CRP), Complement 3 (C3), Complement 4 (C4), IgG, IgA, IgM, plasma sIL-2 R and peripheral T lymphocyte subsets (including CD4(+)CD25(high) regulatory T cells (Treg) and CD4(+)CD25(low+median) effector T cells (Teff)) were analyzed by rate nephelometry immunoassay, chemiluminescence immunoassay and flow cytometry, respectively.
  
  
  RESULTS
  (1) micro-inflammation state in T2DM: Serum CRP, C3, IgA and plasma sIL-2 R were all significantly higher in T2DM than those in healthy control (HC) (all P<0.05). (2) Disturbance of cellular immune in T2DM: Compared with HC, the percentage of peripheral CD3(+)CD4(+)T cells and ratio of CD3(+)CD4(+)T cells to CD3(+)CD8(+)T cells in T2DM were both significantly increased (P<0.05); and the percentage of peripheral CD4(+)CD25(+)T cells, Teff cells increased (P>0.05), Treg cells strikingly decreased in T2DM (P<0.05). A positive correlation between sIL-2R levels and peripheral CD4(+)CD25(+)T cells or Teff cell percentages, as well as a negative correlation between plasma sIL-2 R levels and serum HDL, LDL or CHOL levels in T2DM were shown (all P <0.05).
  
  
  CONCLUSIONS
  Micro-inflammation state in T2DM was characterized by increased sIL-2 R, elevated CD3(+)CD4(+)T cells and the imbalance of Treg cells and Teff cells, which as one of the pathogeneses took part in inflammation reaction in T2DM.
authors.affiliation: Department of Laboratory Medicine, West China Hospital of Sichuan University, Sichuan, PR China.
authors.forename: B
authors.initials: B
authors.lastname: Cai
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.forename: M
authors.initials: M
authors.lastname: Zhang
authors.forename: L
authors.initials: L
authors.lastname: Li
authors.forename: W
authors.initials: W
authors.lastname: Feng
authors.forename: Z
authors.initials: Z
authors.lastname: An
authors.forename: L
authors.initials: L
authors.lastname: Wang
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D003176:Complement C3 / Q000032:analysis; D003181:Complement C4 / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000276:immunology*; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007249:Inflammation / Q000150:complications* / Q000276:immunology*; D008055:Lipids / Q000097:blood; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000097:blood*; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
chemical_list: D003176:Complement C3; D003181:Complement C4; D007070:Immunoglobulin A; D008055:Lipids; D015375:Receptors, Interleukin-2; D002097:C-Reactive Protein