TGF‐β suppresses inflammation through the repression of interleukin‐33 (IL‐33)

Abstract

Transforming growth factor‐β1 (TGF‐β1) is a member of the TGF‐β superfamily of cytokines, which are involved in a wide variety of biological functions such as proliferation, differentiation, migration, and apoptosis. TGF‐β1 binds to a receptor complex and stimulates a set of signaling events leading to changes in gene expression and cell behavior. TGF‐β1 specifically has been shown to be a key player in wound repair and modulation of the immune response. Microarray analysis of normal mouse mammary epithelial cells (NMuMG) treated with TGF‐β1, indicated that the interleukin‐1 family member interleukin‐33 (IL‐33) is repressed by TGF‐β1. IL‐33 is passively released following tissue damage and functions as an alarmin, alerting the immune system to the presence of tissue damage. The goal of this study was to determine if TGF‐β1 decreased the amount of IL‐33 passively released by cells following tissue damage. We utilized previously established methods of inducing passive release of IL‐33 in cell culture. Pretreatment of cells with TGF‐β1 resulted in significantly lower levels of released IL‐33 following induction of tissue damage.These studies may identify a novel therapeutic target for treatment of diseases such as psoriasis, asthma and Crohn's disease. All of these diseases are associated with elevated levels of IL‐33 as well as altered TGF‐β responses. Further investigation of the immune cells affected by repression of IL‐33 could provide information into the specific mechanism of action.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.