Changes in T lymphocyte subsets following injury. Assessment by flow cytometry and relationship to sepsis
- PMID: 3876811
- PMCID: PMC1250971
- DOI: 10.1097/00000658-198511000-00008
Changes in T lymphocyte subsets following injury. Assessment by flow cytometry and relationship to sepsis
Abstract
The increased susceptibility of severely injured patients to infection and death from sepsis has been attributed to abnormalities in cell-mediated immunity. The authors therefore assessed the relative number of peripheral blood T helper cells and T suppressor/cytotoxic cells and total T lymphocytes identified by the monoclonal antibodies (McA) OKT4, OKT8, and OKT3, respectively, in 25 patients with burns from 5 to 85% total body surface area (TBSA) (mean: 40%) and 21 patients with nonthermal injuries (mean Injury Severity Score (ISS): 21.4). Patients were compared to 21 healthy controls. Cells reacting with the McA were detected by flow cytometry, which enabled the examination of a population of cells the size of T lymphocytes, excluding larger contaminating cells that might bind the McA. Patients with burns of 30% TBSA or greater had a significant reduction (p less than or equal to 0.05) in OKT3+ cells up to 50 days post-burn. Both septic and nonseptic burn patients had reduced numbers of OKT3+ cells, as did patients after nonthermal injury, suggesting that this reduction was due to the injury itself. Patients with smaller burns (less than 30% TBSA) as a group did not have reduced OKT4+ cells, whereas those with larger burns showed significant reductions in OKT4+ cells (P less than or equal to 0.05) at 0 to 5, 6 to 10, 11 to 20, 21 to 30, and 41 to 50 days post-burn. Seven burn patients who became septic 10 days post-burn or later had significantly lower OKT4+ cells within 10 days of injury (mean: 33.75% +/- 7.4 SEM) than 10 patients who remained free of sepsis (mean: 42.2% +/- 5.4, p = 0.004). Patients with uncomplicated nonthermal injuries failed to show any significant reduction in OKT4+ cells. Following thermal injury, a reduction in OKT8+ cells was observed up to 10 days in patients with burns less than 30% TBSA, and up to 20 days in patients with larger burns. In both groups, at no time were increased OKT8+ cells found to correlate with clinical events. In patients with nonthermal injury, OKT8+ cells generally remained near the normal range.
Similar articles
-
Depressed immune response in burn patients: use of monoclonal antibodies and functional assays to define the role of suppressor cells.Ann Surg. 1982 Sep;196(3):297-304. doi: 10.1097/00000658-198209000-00008. Ann Surg. 1982. PMID: 6214221 Free PMC article.
-
Autologous and allogeneic mixed-lymphocyte responses following thermal injury in man: the immunomodulatory effects of interleukin 1, interleukin 2, and a prostaglandin inhibitor, WY-18251.Clin Immunol Immunopathol. 1984 Feb;30(2):304-20. doi: 10.1016/0090-1229(84)90064-3. Clin Immunol Immunopathol. 1984. PMID: 6229378
-
Flow cytometric analysis of lymphocyte subpopulations after thermal injury in human beings.Surg Gynecol Obstet. 1984 Jul;159(1):1-8. Surg Gynecol Obstet. 1984. PMID: 6234669
-
Alterations in cell signaling and related effector functions in T lymphocytes in burn/trauma/septic injuries.Shock. 1996 Mar;5(3):157-66. doi: 10.1097/00024382-199603000-00001. Shock. 1996. PMID: 8696979 Review.
-
Pathological changes in the brain after peripheral burns.Burns Trauma. 2023 Feb 6;11:tkac061. doi: 10.1093/burnst/tkac061. eCollection 2023. Burns Trauma. 2023. PMID: 36865685 Free PMC article. Review.
Cited by
-
Reduction in HLA-DR, HLA-DQ and HLA-DP expression by Leu-M3+ cells from the peripheral blood of patients with thermal injury.Clin Exp Immunol. 1989 Mar;75(3):371-5. Clin Exp Immunol. 1989. PMID: 2495202 Free PMC article.
-
Suppression of natural killer-cell function in humans following thermal and traumatic injury.J Clin Immunol. 1986 Jan;6(1):26-36. doi: 10.1007/BF00915361. J Clin Immunol. 1986. PMID: 3485653
-
HLA-DR expression and soluble HLA-DR levels in septic patients after trauma.Ann Surg. 1999 Feb;229(2):246-54. doi: 10.1097/00000658-199902000-00013. Ann Surg. 1999. PMID: 10024107 Free PMC article.
-
The compensatory anti-inflammatory response syndrome (CARS) in critically ill patients.Clin Chest Med. 2008 Dec;29(4):617-25, viii. doi: 10.1016/j.ccm.2008.06.010. Clin Chest Med. 2008. PMID: 18954697 Free PMC article. Review.
-
Pathophysiological dynamics in the contact, coagulation, and complement systems during sepsis: Potential targets for nafamostat mesilate.J Intensive Med. 2024 Apr 10;4(4):453-467. doi: 10.1016/j.jointm.2024.02.003. eCollection 2024 Oct. J Intensive Med. 2024. PMID: 39310056 Free PMC article. Review.
References
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical