The role of IL‐22 in the resolution of sterile and nonsterile inflammation

Abstract

In a broad sense, inflammation can be conveniently characterised by two phases: the first phase, which is a pro‐inflammatory, has evolved to clear infection and/or injured tissue; and the second phase concerns regeneration of normal tissue and restitution of normal physiology. Innate immune cell‐derived pro‐inflammatory cytokines and chemokines activate and recruit nonresident immune cells to the site of infection, thereby amplifying the inflammatory responses to clear infection or injury. This phase is followed by a cytokine milieu that promotes tissue regeneration. There is no absolute temporal distinction between these two phases, and cytokines may have dual pleiotropic effects depending on the timing of release, inflammatory microenvironment or concentrations. IL‐22 is a cytokine with reported pro‐ and anti‐inflammatory roles; in this review, we contend that this protein has primarily a function in restitution of normal tissue and physiology.

IL-22 induced cell extrusion and IL-18-induced pyroptosis prevent and cure rotavirus infection

“…A key aspect of this process is that it permits elimination of cells without comprising gut barrier function and thus avoiding infectious and inflammation that might otherwise result therefrom. Accordingly, administration of IL-22 is associated with few adverse effects and in a variety of scenarios shows clear ability to resolve inflammation [24].…”

Dissecting pharmacological effects of chloroquine in cancer treatment: interference with inflammatory signaling pathways

“…45 Therefore, a combination with inhibitors of DNA repair can be studied, as under certain conditions it might improve Th1-driven immune responses, and in parallel, provide additional cytotoxicity toward malignant cells. 282 In normal and tumor tissue alike, the activity of STAT3 itself affects vascularity and pericyte interactions with their microenvironment, including myeloid cells. 197,281 In normal tissues, STAT3 would protect from excessive Th1 activity and inflammation.…”

“…197,281 In normal tissues, STAT3 would protect from excessive Th1 activity and inflammation. 282 In normal and tumor tissue alike, the activity of STAT3 itself affects vascularity and pericyte interactions with their microenvironment, including myeloid cells. [283][284][285][286] However, unlike malignant tissue niches, normal tissue uses the intact regulatory network of STAT3 and NF-jB as a common mechanism to recover from inflammation.…”

Interleukin-22 from bench to bedside: a promising drug for epithelial repair

“…6,7,12 However, IL-22 has also been implicated in promoting inflammation under certain conditions, 12 which raises some concerns about IL-22 therapy. The study from Tang et al 2 revealed that IV injection of F-652 induced dose-dependent increases in serum acute-phase proteins, including serum amyloid A and C-reactive proteins, but did not alter serum levels of a large number of pro-inflammatory cytokines/chemokines even at the highest dose of F-652 (45 µg/kg).…”