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Regulation of Interleukin 33 by Transforming Growth Factor‐β in Epithelia Cells, Fibroblasts and Keratinocytes
Author(s) -
Woelfel Jennifer M,
DenHaese Jason P,
Gervasi Megan E,
Ruvio Stacy
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.908.11
Subject(s) - microbiology and biotechnology , cytokine , stromal cell , interleukin 33 , transforming growth factor , immune system , biology , immunology , angiogenesis , transforming growth factor beta , interleukin , cancer research
Interleukin 33 (IL‐33), a member of the IL‐1 family of cytokines, plays a key role in inflammatory responses functioning as an alarmin, alerting the immune system to tissue damage. IL‐33 signaling molecules following damage, IL‐33 coordinates recruitment and activation of immune cells leading to the release of mediators such as VEGF, which drives angiogenesis and skin remodeling.I L‐33 is expressed in epithelial cells, stromal cells, and endothelial cells. High levels of IL‐33 as has been implicated in diseases such as asthma, inflammatory skin and rheumatological diseases. Preliminary studies have shown that the pluripotent cytokine Transforming Growth Factor‐β (TGF‐β) represses expression of IL‐33 in mouse and human mammary epithelial cells, human kidney and lung epithelial cells and human primary fibroblast in vitro. TGF‐β is a cytokine involved in a number of cellular responses including cell differentiation, growth inhibition, extracellular matrix sti mulation, immunosuppression, and immunomodulation. Our current studies revealed that repression of IL‐33 was dependent on the TGF‐β canonical pathway of signaling. Continuing studies will utilize mast cells to determine the biological implications of repression of IL‐33 by TGF‐β. Support or Funding Information Work supported by the Department of Biology and Mathematics, D'Youville College.