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An interesting phenomenon of chronic inflammation is that the associated cytokines can simultaneously promote inflammatory cell recruitment and tissue pathology as well as tissue regeneration and development of inducible organized lymphoid tissues (tertiary lymphoid organs or TLO), demonstrating the remarkable dynamics of the immune interactions with host tissues. In mucosal tissues, chronic immune-mediated inflammation can present a mixed inflammatory pathology including neutrophil infiltrates along with the lymphocytic aggregates. The factors driving this pattern may involve effects on barrier function as well as inducible mechanisms associated with immune surveillance. The relative contribution of these factors may be important in determining the outcome, from resolution to inflammatory stalemate to progressive tissue pathology and destruction. Here, we focus on the specific impact of cytokine-driven inducible lymphoid cells and tissues on immune surveillance at mucosal surfaces, including the induction of epithelial M cells. We propose a model of chronic intestinal inflammation to assess the relative contributions of mucosal barrier integrity, M cell transcytosis of luminal microbes, and inducible lymphoid tissues.

Scar formation, a physiologic process in adult wound healing, can have devastating effects for patients; a multitude of pathologic outcomes, affecting all organ systems, stems from an amplification of this process. In contrast to adult wound repair, the early-gestation fetal skin wound heals without scar formation, a phenomenon that appears to be intrinsic to fetal skin. An intensive research effort has focused on unraveling the mechanisms that underlie scarless fetal wound healing in an attempt to improve the quality of healing in both children and adults. Unique properties of fetal cells, extracellular matrix, cytokine profile, and gene expression contribute to this scarless repair. Despite the great increase in knowledge gained over the past decades, the precise mechanisms regulating scarless fetal healing remain unknown. Herein, we describe the current proposed mechanisms underlying fetal scarless wound healing in an effort to recapitulate the fetal phenotype in the postnatal environment., (Copyright © 2012 Wiley Periodicals, Inc.)