Immune-Mediated Repair: A Matter of Plasticity

Abstract

Though the immune system is generally defined as a system of defense, it is increasingly recognized that the immune system also plays a crucial role in tissue repair and its potential dysregulations. In this review, we explore how distinct immune cell types are involved in tissue repair and how they interact in a process that is tightly regulated both spatially and temporally. We insist on the concept of immune cell plasticity which, in recent years, has proved fundamental for the success/understanding of the repair process. Overall, the perspective presented here suggests that the immune system plays a central role in the physiological robustness of the organism, and that cell plasticity contributes to the realization of this robustness.

Keywords: fibrosis; innate lymphoid cells; macrophages; neutrophils; plasticity; repair; robustness; transdifferentiation.

Figure 1

The roles of immune cells (colored) during the three phases of tissue repair: inflammation (red), new tissue formation (green), and remodeling (purple). Tissue repair is driven by interactions between immune cells and other cell types such as fibroblasts (not colored), as well the temporary plasticity of immune cells, e.g., macrophage switch from an inflammatory phenotype (red) to a tissue repair phenotype (green) to a resolving phenotype (purple).

Figure 2

Relative importance of inflammation, new tissue formation, and remodeling in three different situations. In normal wound healing, inflammation (1, in red), new tissue formation (2, in green), and remodeling (3, in purple) are at a basal level. In ulcers, inflammation and new tissue formation are at higher levels, whereas remodeling is lower than the basal level. In fibrosis, inflammation, new tissue formation, and remodeling are all higher than their basal levels.