Only a subset of trauma patients with depressed mitogen responses have true T cell dysfunctions.

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.