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. 2003 Jan 12:5:13-35.

PATHOLOGICAL ASPECTS OF THE ANTI-INFLAMMATORY/IMMUNE SUPPRESSIVE RESPONSE IN SEPSIS AND SHOCK

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PATHOLOGICAL ASPECTS OF THE ANTI-INFLAMMATORY/IMMUNE SUPPRESSIVE RESPONSE IN SEPSIS AND SHOCK

Alfred Ayala et al. Rec Res Dev Immunol. .

Abstract

Despite the recent advances in contemporary therapeutic, operative as well as supportive care sepsis and its associated co-morbidity/mortality are still a common occurrence in the critically ill trauma/surgical patient. Thus, it remains important to continue to expand our understanding of pathological components which drive the development of immune dysfunction contributing to subsequent multiple organ failure. Here we overview some of the immuno-pathological processes, cells and mediators which may play a role in the development of this immune dysfunctional condition.

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Figures

Figure 1
Figure 1
Postulated steps at which there exist some evidence that the process of neutrophil (A), macrophage (B) or T-cell (C) activation/differentiation appears to be inhibited or might be a target of suppression following the onset of sepsis or injury. [1] Dispution of activational signal; [2] active anti-inflammatory induced suppression; [3] maladaptive intracellular signaling; [4] deactivation driven by immune suppressive and/or regulatory cell population; and [5] pathologic induction of apoptosis.
Figure 2A
Figure 2A
Diagrammatical representation of the various anti-inflammatory intracellular signaling pathways (— ▶) and their inducers which for the most part inhibit immune cell activation (A). Pathways that appear to be involved in transmitting signals that both stimulate and inhibit cell activation are indicated by = ▶. (B) Some of the key components, mediators and pathways (mitochondrial, endoplasmic reticulum [ER] and death receptor pathways) that have been implicated in the induction and suppression of immune cell apoptosis.

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