title: Only a subset of trauma patients with depressed mitogen responses have true T cell dysfunctions.
abstract: Many studies have demonstrated depressed mitogenic responses in trauma/burn patients' peripheral blood mononuclear cells (PBMC). However, data attributing the relative contribution of secreted inhibitory factors versus a true T cell dysfunction to these depressed mitogenic responses have been conflicting. We have characterized the T cell dysfunctions in posttrauma mitogen depression by simultaneously assessing patient T cell proliferation in the phytohemagglutinin-stimulated PBMC and in the purified T cell population induced with anti-CD3 + anti-CD4. Patients' samples showed three distinct patterns or progressive phases of T cell responses: (i) normal or elevated T cell proliferation in both the whole PBMC and the isolated T cell population (phase I); (ii) depressed T cell proliferation in the PBMC but normal, or even elevated, proliferation in the isolated T cell population (phase II); and (iii) depressed T cell proliferation in both the PBMC and the isolated T cell population (phase III). Patients whose T cells exhibited only a phase I response experienced no major complications with a positive clinical outcome. Patients whose T cell alterations progressed to phase II experienced infectious episodes and some complications, but all had positive clinical outcomes. In contrast, patients whose T cells progressed to phase III dysfunction had severe clinical complications (multiple organ failure), with a negative clinical outcome (80% mortality). Patients whose T cells had a phase I or phase II response pattern had no true T cell dysfunctions in the absence of monocytes. However, patients whose T cells had a true T cell dysfunction (phase III) response pattern were at high risk for mortality. Thus, a true T cell dysfunction, though occurring in only a minority of trauma patients, is predictive of clinical outcome.
authors.affiliation: University of Massachusetts Medical Center, Department of Surgery, Worcester 01655, USA.
authors.forename: A K
authors.initials: AK
authors.lastname: De
authors.forename: K
authors.initials: K
authors.lastname: Kodys
authors.forename: J C
authors.initials: JC
authors.lastname: Puyana
authors.forename: G
authors.initials: G
authors.lastname: Fudem
authors.forename: J
authors.initials: J
authors.lastname: Pellegrini
authors.forename: C L
authors.initials: CL
authors.lastname: Miller-Graziano
mesh_terms: D000293:Adolescent; D000328:Adult; D002056:Burns / Q000276:immunology; D015232:Dinoprostone / Q000097:blood; D005260:Female; D006801:Humans; D007108:Immune Tolerance; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D014947:Wounds and Injuries / Q000276:immunology*
chemical_list: D016753:Interleukin-10; D007371:Interferon-gamma; D015232:Dinoprostone