Journal
CELLULAR IMMUNOLOGY
Volume 343, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2017.12.014
Keywords
Interleukin-33; ST2L; sST2; Colorectal cancer; Ulcerative colitis; Inflammatory tumor microenvironment
Categories
Funding
- MEXT KAKENHI [23112510]
- JSPS KAKENHI [24791422, 16K21177, 25430110, 16K10594]
- Shimane University SUIGANN Project
- Japan Arteriosclerosis Research Foundation
- Grants-in-Aid for Scientific Research [24791422, 25430110, 16K10594] Funding Source: KAKEN
Ask authors/readers for more resources
Interleukin-33 (IL-33) has been identified as a natural ligand of ST2L. IL-33 primarily acts as a key regulator of Th2 responses through binding to ST2L, which is antagonized by soluble ST2 (sST2). The IL-33/ST2L axis is involved in various inflammatory pathologies, including ulcerative colitis (UC). Several recent investigations have also suggested that the IL-33/ST2L axis plays a role in colorectal cancer (CRC) progression. In CRC, tumorand stroma-derived IL-33 may activate ST2L on various cell types in an autocrine and paracrine manner. Although several findings support the hypothesis that the IL-33/ST2L axis positively regulates CRC progression, other reports do not; hence, this hypothesis remains controversial. At any rate, recent studies have provided overwhelming evidence that the IL-33/ST2L axis plays important roles in CRC progression. This review summarizes the role of the IL-33/ST2L axis in the UC and CRC microenvironments.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available