PMID- 31867327
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 2296-634X (Print)
IS  - 2296-634X (Electronic)
IS  - 2296-634X (Linking)
VI  - 7
DP  - 2019
TI  - Function and Regulation of IL-36 Signaling in Inflammatory Diseases and Cancer 
      Development.
PG  - 317
LID - 10.3389/fcell.2019.00317 [doi]
LID - 317
AB  - The IL-36 subfamily of cytokines belongs to the IL-1 superfamily and consists of 
      three pro-inflammatory agonists IL-36alpha, IL-36beta, IL-36gamma, and an IL-36 receptor 
      (IL-36R) antagonist, IL-36Ra. These IL-36 cytokines function through a common 
      receptor to modulate innate and adaptive immune responses. IL-36 cytokines are 
      expressed as inactive precursors and require proteolytic processing to become 
      fully active. Upon binding to IL-36R, IL-36 agonists augment the expression and 
      production of inflammatory cytokines via activating signaling pathways. IL-36 is 
      mainly expressed in epidermal, bronchial, and intestinal epithelial cells that 
      form the barrier structures of the body and regulates the balance between 
      pro-inflammatory and anti-inflammatory cytokine production at these tissue sites. 
      Dysregulation of IL-36 signaling is a major etiological factor in the development 
      of autoimmune and inflammatory diseases. Besides its critical role in 
      inflammatory skin diseases such as psoriasis, emerging evidence suggests that 
      aberrant IL-36 activities also promote inflammatory diseases in the lung, 
      kidneys, and intestines, underscoring the potential of IL-36 as a therapeutic 
      target for common inflammatory diseases. The role of IL-36 signaling in cancer 
      development is also under investigation, with limited studies suggesting a 
      potential anti-tumor effect. In this comprehensive review, we summarize current 
      knowledge regarding the expression, activation, regulatory mechanisms, and 
      biological functions of IL-36 signaling in immunity, inflammatory diseases, and 
      cancer development.
CI  - Copyright (c) 2019 Queen, Ediriweera and Liu.
FAU - Queen, Dawn
AU  - Queen D
AD  - Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, 
      United States.
FAU - Ediriweera, Chathumadavi
AU  - Ediriweera C
AD  - The Hormel Institute, University of Minnesota, Austin, MN, United States.
FAU - Liu, Liang
AU  - Liu L
AD  - The Hormel Institute, University of Minnesota, Austin, MN, United States.
LA  - eng
GR  - K01 AR064315/AR/NIAMS NIH HHS/United States
GR  - P30 AR044535/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20191204
PL  - Switzerland
TA  - Front Cell Dev Biol
JT  - Frontiers in cell and developmental biology
JID - 101630250
PMC - PMC6904269
OTO - NOTNLM
OT  - IL-36 signaling
OT  - cancer
OT  - cytokine
OT  - inflammation
OT  - psoriasis
EDAT- 2019/12/24 06:00
MHDA- 2019/12/24 06:01
PMCR- 2019/01/01
CRDT- 2019/12/24 06:00
PHST- 2019/09/05 00:00 [received]
PHST- 2019/11/20 00:00 [accepted]
PHST- 2019/12/24 06:00 [entrez]
PHST- 2019/12/24 06:00 [pubmed]
PHST- 2019/12/24 06:01 [medline]
PHST- 2019/01/01 00:00 [pmc-release]
AID - 10.3389/fcell.2019.00317 [doi]
PST - epublish
SO  - Front Cell Dev Biol. 2019 Dec 4;7:317. doi: 10.3389/fcell.2019.00317. eCollection 
      2019.