PMID- 36376594
OWN - NLM
STAT- MEDLINE
DCOM- 20230127
LR  - 20230222
IS  - 1435-5922 (Electronic)
IS  - 0944-1174 (Linking)
VI  - 58
IP  - 2
DP  - 2023 Feb
TI  - Pro- and anti-inflammatory roles of interleukin (IL)-33, IL-36, and IL-38 in 
      inflammatory bowel disease.
PG  - 69-78
LID - 10.1007/s00535-022-01936-x [doi]
AB  - Interleukin-33 (IL-33), IL-36, and IL-38 are members of the IL-1 cytokine family. 
      The expression of each cytokine has been reported to be increased in the inflamed 
      mucosa of patients with inflammatory bowel disease (IBD). IL-33 and IL-36 have 
      been studied for pro- and anti-inflammatory functions, and IL-38 has been 
      characterized as an anti-inflammatory cytokine by antagonizing the IL-36 receptor 
      (IL-36R). IL-33 is a nuclear cytokine constitutively expressed by certain cell 
      types such as epithelial, endothelial, and fibroblast-like cells and released on 
      necrotic cell death. IL-33 mainly induces type 2 immune response through its 
      receptor suppression tumorigenicity 2 (ST2) from Th2 cells and type 2 innate 
      lymphoid cells (ILC2s), but also by stimulating Th1 cells, regulatory T cells, 
      and CD8(+) T cells. IL-36 cytokines consist of three agonists: IL-36alpha, IL-36beta, 
      and IL-36gamma, and two receptor antagonists: IL-36R antagonist (IL-36Ra) and IL-38. 
      All IL-36 cytokines bind to the IL-36R complex and exert various functions 
      through NF-kappaB and mitogen-activated protein kinase (MAPK) pathways in 
      inflammatory settings. IL-33 and IL-36 also play a crucial role in intestinal 
      fibrosis characteristic manifestation of CD. In this review, we focused on the 
      current understanding of the pro- and anti-inflammatory roles of IL-33, IL-36, 
      and IL38 in experimental colitis and IBD patients.
CI  - (c) 2022. Japanese Society of Gastroenterology.
FAU - Andoh, Akira
AU  - Andoh A
AUID- ORCID: 0000-0001-8533-2669
AD  - Department of Medicine, Shiga University of Medical Science, Seta-Tsukinowa, 
      Otsu, Shiga, 520-2192, Japan. andoh@belle.shiga-med.ac.jp.
FAU - Nishida, Atsushi
AU  - Nishida A
AD  - Department of Medicine, Shiga University of Medical Science, Seta-Tsukinowa, 
      Otsu, Shiga, 520-2192, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20221114
PL  - Japan
TA  - J Gastroenterol
JT  - Journal of gastroenterology
JID - 9430794
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-33)
RN  - 0 (Cytokines)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (IL-38 protein, human)
RN  - 0 (Interleukins)
SB  - IM
MH  - Humans
MH  - *Interleukin-1/metabolism
MH  - Interleukin-33
MH  - Immunity, Innate
MH  - CD8-Positive T-Lymphocytes
MH  - Lymphocytes
MH  - *Inflammatory Bowel Diseases/metabolism
MH  - Cytokines
MH  - Anti-Inflammatory Agents
MH  - Interleukins
OTO - NOTNLM
OT  - Alarmin
OT  - Cytokines
OT  - Fibrosis
OT  - IL-1RAcP
OT  - ST2
EDAT- 2022/11/15 06:00
MHDA- 2023/01/28 06:00
CRDT- 2022/11/14 23:58
PHST- 2022/09/28 00:00 [received]
PHST- 2022/10/29 00:00 [accepted]
PHST- 2022/11/15 06:00 [pubmed]
PHST- 2023/01/28 06:00 [medline]
PHST- 2022/11/14 23:58 [entrez]
AID - 10.1007/s00535-022-01936-x [pii]
AID - 10.1007/s00535-022-01936-x [doi]
PST - ppublish
SO  - J Gastroenterol. 2023 Feb;58(2):69-78. doi: 10.1007/s00535-022-01936-x. Epub 2022 
      Nov 14.