Simultaneous aberrations in MØ and T cell function adversely affect trauma patients' clinical outcome: A possible faulty IL-13 feedback loop

Possible defective trauma patients' MØ-T-cell feedback interactions between T cell IL-13 production and IL-1β and IL-18 MØ secretion were assessed. MØ produced IL-1 and IL-18 augment T cell IL-13, which in turn limits excessive macrophage activation. Immunodepressed patients' T cells (depressed proliferation to αCD3 + αCD4) had decreased IL-13 production concomitant to aberrant MØ activities (↑mTNFα, ↓IL-10) and consequent multiple organ failure (MOF). Decreased IL-13 levels in patients' T cell and diminished MØ supernatant augmentation of healthy controls' T cell IL-13 production appeared concomitantly, suggesting patients' aberrant monokine levels might intensify in vivo T cell dysfunction severity. Patients' MØ supernatants, which failed to augment controls' T cell IL-13 production, had depressed IL-1β and lower induction of IL-18 than immunocompetent patients' MØ, but combined addition of IL-1β and IL-18 restored these MØs' IL-13 enhancing activity. These data suggest that immunodepressed patients' aberrant monokine and depressed T cell IL-13 production are independent but synergistic contributors to emergence of MOF.