title: Selective defects of T lymphocyte function in patients with lethal intraabdominal infection.
abstract: BACKGROUND
  In recent models, compensatory antiinflammatory immune reactions triggered in response to systemic inflammation were considered important for the outcome of sepsis. The present study investigated T-cell functions in patients with postoperative sepsis due to intra-abdominal infection.
  
  
  METHODS
  Peripheral T cells were purified from 32 sepsis patients and 41 healthy controls. Proliferation and production of interferon (IFN)-gamma, interleukin (IL)-2, IL-4, tumor necrosis factor (TNF), and IL-10 were stimulated by cross-linking of CD3 and CD28.
  
  
  RESULTS
  T-cell proliferation and production of IL-2 and TNF were severely suppressed in patients with lethal intraabdominal infection as compared with survivors and healthy controls. Sepsis survivors showed normal T-cell proliferation and IL-2 release, whereas secretion of TNF was reduced. However, TNF suppression in survivors was less severe than in nonsurviving patients. Defective T-cell functions were observed at the onset of sepsis and persisted throughout the entire observation period. T-cell production of IL-4 and IL-10 was not affected by postoperative intraabdominal infection.
  
  
  CONCLUSIONS
  Defective T-cell proliferation and secretion of IL-2 and TNF correlate with sepsis mortality, thus indicating an important role of T 'cells for the immune defense against postoperative infection. Immune defects were evident at the onset of sepsis, suggesting that immunosuppression may develop as a primary response to sepsis without preceding immune hyperactivity.
authors.affiliation: Department of Surgery, Klinikum rechts der Isar, Technische Universität, Munich, Germany.
authors.forename: C D
authors.initials: CD
authors.lastname: Heidecke
authors.forename: T
authors.initials: T
authors.lastname: Hensler
authors.forename: H
authors.initials: H
authors.lastname: Weighardt
authors.forename: N
authors.initials: N
authors.lastname: Zantl
authors.forename: H
authors.initials: H
authors.lastname: Wagner
authors.forename: J R
authors.initials: JR
authors.lastname: Siewert
authors.forename: B
authors.initials: B
authors.lastname: Holzmann
mesh_terms: D000005:Abdomen; D000368:Aged; D002455:Cell Division; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D007378:Interleukins / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications / Q000276:immunology / Q000503:physiopathology*; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology / Q000503:physiopathology*; D013601:T-Lymphocytes / Q000276:immunology / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma