title: The "T" in trauma: the helper T-cell response and the role of immunomodulation in trauma and burn patients.
abstract: BACKGROUND
  The immune system undergoes numerous changes after traumatic and burn injuries, including a down-regulation of the TH1 response and up-regulation of the TH2 response.
  
  
  METHODS
  The PubMed, Medline, and Ovid search engines were queried for relevant human studies. Bibliographies were also meticulously reviewed.
  
  
  RESULTS
  An interesting and potentially clinically relevant pattern of immune dysregulation exists after injury. The type 1 T-helper cell (TH1) response is suppressed as illustrated by diminished interleukin (IL)-2, interferon (IFN)-gamma, and IL-12 levels after major injury. The enhancement of the TH2 response is marked by elevated IL-10 and IL-4. Certain cytokine profiles, ratios, and polymorphisms may help identify patients at increased risk of systemic inflammatory response syndrome (SIRS), sepsis, multiple organ failure (MOF), and deep venous thrombosis. The most promising prognostic indicators to date are decreased production of the IL-12, elevated IL-10, soluble IL-2 receptor-a (sIL-2Ra), and IL-18 levels, IL-18 promoter polymorphisms, the IL-6:IL-10 ratio, and the degree of TH1 suppression as measured by diminished IL-2 and IFN-gamma. The Cytokine sections are subdivided into basic science, human studies, animal studies (when necessary), and directed therapeutics. The outcomes of sepsis, SIRS, or MOF are generally discussed together.
  
  
  CONCLUSIONS
  T-cell-specific immunologic changes occur after major injury. Identification of those TH1/TH2 cytokine profiles associated with worse prognosis may one day allow clinicians to risk stratify injured patients and identify those at increased risk of developing SIRS, sepsis, MOF, and deep venous thrombosis. Immune-targeted therapies may eventually serve as effective treatments in the acute setting to decrease morbidity and mortality, and to improve the management and prognosis of those patients at risk for developing postinjury complications.
authors.affiliation: Department of Emergency Medicine and Internal Medicine, The State University of New York Downstate Medical Center and Kings County Hospital Center, Brooklyn, New York, USA. andrewcmiller@optonline.net
authors.forename: Andrew C
authors.initials: AC
authors.lastname: Miller
authors.forename: Rashid M
authors.initials: RM
authors.lastname: Rashid
authors.forename: Elamin M
authors.initials: EM
authors.lastname: Elamin
mesh_terms: D015415:Biomarkers; D002056:Burns / Q000276:immunology*; D006801:Humans; D007155:Immunologic Factors / Q000276:immunology / Q000502:physiology; D007372:Interferons / Q000276:immunology* / Q000502:physiology; D007378:Interleukins / Q000276:immunology* / Q000502:physiology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000502:physiology; D014947:Wounds and Injuries / Q000276:immunology*
chemical_list: D015415:Biomarkers; D007155:Immunologic Factors; D007378:Interleukins; D007372:Interferons