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Review
. 2003 Aug;31(8 Suppl):S558-71.
doi: 10.1097/01.CCM.0000081438.04801.D9.

Mechanisms of immune resolution

Alfred Ayala  1 , Chun-Shiang Chung, Patricia S Grutkoski, Grace Y Song
Affiliations
Review

Mechanisms of immune resolution

Alfred Ayala et al. Crit Care Med. 2003 Aug.

Abstract

Initially after injury, the innate/proinflammatory and some aspects of the acquired immune response are up-regulated to maintain a defense against foreign pathogens, clear tissue debris present at the wound site, and orchestrate aspects of tissue remodeling, cell proliferation and angiogenic process, associated with the wound response. However, for proper wound healing to progress, this initial inflammatory response has to be regulated or shut down so as to allow for the reestablishment of matrix, recellularization, and tissue remodeling. Inability to properly resolve the extent of innate/acquired response at a site of injury can lead to poor wound healing, immune suppression, and recurrent infectious episodes. This review attempts to summarize information on regulatory mechanisms that are thought to be involved in controlling/resolving innate or acquired immune responses so as to provide a framework for use in thinking about the impact these processes and their manipulation may have on wound healing and its potential management.

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Figures

Figure 1
Figure 1
Postulated steps at which the process of neutrophil (A), macrophage (B) or T-cell (C) activation/differentiation might be inhibited.
Figure 2
Figure 2
Diagrammatic representation of the various anti-inflammatory intracellular signaling pathways (→) and their inducers, which, for the most part, inhibit immune cell activation. Pathways that seem to be involved in transmitting signals that both stimulate and inhibit cell activation are indicated by formula image.
Figure 3
Figure 3
Postulated interrelationship of macrophages (M), dendritic cells, neutrophils (PMN), T lymphocytes (Th0, Th1, Th2, Th3, NK-T cell or Tc1, Tc2 cells), their general activational stimuli, and the cytokines they express to the regulation/development of a competent cell-mediated immune response.
Figure 4
Figure 4
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.
See this image and copyright information in PMC

References

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Publication types

MeSH terms