PMID- 22374445
OWN - NLM
STAT- MEDLINE
DCOM- 20120507
LR  - 20191112
IS  - 1349-7413 (Electronic)
IS  - 0911-4300 (Linking)
VI  - 35
IP  - 1
DP  - 2012
TI  - [Regulation of inflammation through JAK3-Stat6 pathway in dendritic cells].
PG  - 62-8
AB  - Dendritic cells (DCs) is the cell that act as source of the immune response by 
      exquisitely presenting antigens to acquired immunity such as the T cells. Janus 
      kinase (JAK) is a tyrosine kinase that is activated immediately after the 
      cytokine binds to its unique receptor expressed on the cell surface. Among the 
      JAKs, expression of JAK3 is limited on haematopoietic cells and is indispensable 
      for lymphocyte development and proliferation. We have demonstrated that 
      JAK3-deficient DCs normally develop, uptake antigens, produce inflammatory 
      cytokines and function as an antigen-presenting cell, although they over-produce 
      IL-10. Among the transcription factors that are known to be activated by JAK3, we 
      explored the phenotype of Stat6-deficient DCs which is a transcription factor 
      specifically activated by JAK3. Interestingly, development, function and 
      inflammatory cytokine production was normal with over-production of IL-10 which 
      was in line with the JAK3-deficient DCs. IL-4 is well known to activate 
      JAK3-Stat6 in the cytoplasm and has been reported to be produced in the synovial 
      fluid of rheumatoid arthritis patients. Hence the suppression of IL-10 production 
      by IL-4 can be considered as one of the inflammatory process of arthritis. 
      Moreover, induction of IL-10 production by DCs can be one mechanism of action of 
      the JAK inhibitor (tofacitinib) which have shown high efficiency on active 
      rheumatoid arthritis in clinical trials.
FAU - Yamaoka, Kunihiro
AU  - Yamaoka K
AD  - The First Department of Internal Medicine, School of Medicine, University of 
      Occupational and Enviromental Health, Kitakyushu, Japan.
FAU - Maeshima, Keisuke
AU  - Maeshima K
FAU - Kubo, Satoshi
AU  - Kubo S
FAU - Tanaka, Yoshiya
AU  - Tanaka Y
LA  - jpn
PT  - English Abstract
PT  - Journal Article
PT  - Review
PL  - Japan
TA  - Nihon Rinsho Meneki Gakkai Kaishi
JT  - Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology
JID - 9505992
RN  - 0 (Interleukins)
RN  - 0 (STAT6 Transcription Factor)
RN  - 0 (STAT6 protein, human)
RN  - EC 2.7.10.2 (Janus Kinase 3)
SB  - IM
MH  - Animals
MH  - Dendritic Cells/*immunology/metabolism
MH  - Humans
MH  - Inflammation/*immunology/metabolism
MH  - Interleukins/biosynthesis/immunology
MH  - Janus Kinase 3/immunology/metabolism
MH  - STAT6 Transcription Factor/immunology/metabolism
MH  - *Signal Transduction
EDAT- 2012/03/01 06:00
MHDA- 2012/05/09 06:00
CRDT- 2012/03/01 06:00
PHST- 2012/03/01 06:00 [entrez]
PHST- 2012/03/01 06:00 [pubmed]
PHST- 2012/05/09 06:00 [medline]
AID - JST.JSTAGE/jsci/35.62 [pii]
AID - 10.2177/jsci.35.62 [doi]
PST - ppublish
SO  - Nihon Rinsho Meneki Gakkai Kaishi. 2012;35(1):62-8. doi: 10.2177/jsci.35.62.