Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Interleukin-33 and Obesity-Related inflammation and Cancer

Version 1 : Received: 3 September 2024 / Approved: 3 September 2024 / Online: 3 September 2024 (23:28:39 CEST)

How to cite: Kowitt, C.; Zhang, Q. Interleukin-33 and Obesity-Related inflammation and Cancer. Preprints 2024, 2024090252. https://doi.org/10.20944/preprints202409.0252.v1 Kowitt, C.; Zhang, Q. Interleukin-33 and Obesity-Related inflammation and Cancer. Preprints 2024, 2024090252. https://doi.org/10.20944/preprints202409.0252.v1

Abstract

Obesity and chronic inflammation are well-known risk factors for cancer. Interleukin-33 (IL-33) functions in inflammatory diseases, particularly those related to obesity and cancer. However, the correlation and molecular mechanisms linking IL-33, obesity, and cancer remain unclear. IL-33 is a nuclear cytokine released as an alarm signal when cells are damaged or stressed. It is expressed in epithelial, endothelial, and fibroblast-like cells during normal conditions and in-flammation. When IL-33 is present, immune cells expressing the IL-1RL1/ST2 receptor are alerted in response to tissue damage or cell injury. Research on IL-33 and its correlation with obesity has revealed improvements in inflammatory and metabolic changes associated with obesity. IL-33 can have both pro-tumorigenic and antitumorigenic effects, depending on the cellular content, in-flammatory environment, expression levels, and bioactivity of IL-33. This review will discuss the various functions of IL-33 in obesity-driven inflammation and cancers and how they intersect.

Keywords

IL-33; ST2; Immune Cells; Inflammation; Obesity; Cancer

Subject

Biology and Life Sciences, Life Sciences

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