IL‑33 and kidney disease (Review).

Abstract:

:Interleukin (IL)-33, is a novel member of the IL-1 superfamily, and act as a dual-function molecule as a nuclear factor and cytokine. The expression of IL-33 can be detected in several tissues and cells in humans and in mice. In addition to the conventional secretion approach for cytokines, full-length IL-33 can also be released into the extracellular space following cell damage or mechanical injury. IL-33 mediates its biological effects by interacting with the receptors, suppression of tumorigenicity 2 (ST2) and IL-1 receptor accessory protein, activating intracellular molecules in the nuclear factor-κB and mitogen-activated protein kinase signaling pathways, which drive the production of type 2 cytokines, including IL-4, IL-5 and IL-3, from polarized T helper 2 cells. Increasing evidence indicates that IL-33 is important in chronic kidney disease, and may be involved in the progression of renal fibrosis associated with systemic lupus erythematosus and renal graft damage. In addition, IL-33 contributes to acute kidney injury. In the present review, the biology of IL-33, and the association of IL-33 with kidney diseases are discussed.

journal_name

Mol Med Rep

authors

Yang F,Zhu P,Duan L,Yang L,Wang J

doi

10.3892/mmr.2015.4516

subject

Has Abstract

pub_date

2016-01-01 00:00:00

pages

3-8

issue

1

eissn

1791-2997

issn

1791-3004

journal_volume

13

pub_type

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