PMID- 25654487
OWN - NLM
STAT- MEDLINE
DCOM- 20151228
LR  - 20171116
IS  - 1555-3892 (Electronic)
IS  - 0963-6897 (Linking)
VI  - 24
IP  - 3
DP  - 2015
TI  - Irisflorentin modifies properties of mouse bone marrow-derived dendritic cells 
      and reduces the allergic contact hypersensitivity responses.
PG  - 573-88
LID - 10.3727/096368915X687002 [doi]
AB  - Irisflorentin is an isoflavone component derived from the roots of Belamcanda 
      chinensis (L.) DC. In traditional Chinese medicine, this herb has pharmacological 
      properties to treat inflammatory disorders. Dendritic cells (DCs) are crucial 
      modulators for the development of optimal T-cell immunity and maintenance of 
      tolerance. Aberrant activation of DCs can induce harmful immune responses, and so 
      agents that effectively improve DC properties have great clinical value. We 
      herein investigated the effects of irisflorentin on lipopolysaccharide 
      (LPS)-stimulated maturation of mouse bone marrow-derived DCs in vitro and in the 
      contact hypersensitivity response (CHSR) in vivo. Our results demonstrated that 
      treatment with up to 40 muM irisflorentin does not cause cellular toxicity. 
      Irisflorentin significantly lessened the proinflammatory cytokine production 
      (tumor necrosis factor-alpha, interleukin-6, and interleukin-12p70) by LPS-stimulated 
      DCs. Irisflorentin also inhibited the expression of LPS-induced major 
      histocompatibility complex class II and costimulatory molecules (CD40 and CD86) 
      on LPS-stimulated DCs. In addition, irisflorentin diminished LPS-stimulated 
      DC-elicited allogeneic T-cell proliferation. Furthermore, irisflorentin 
      significantly interfered with LPS-induced activation of IkappaB kinase, c-Jun 
      N-terminal kinase, and p38, as well as the nuclear translocation of NF-kappaB p65. 
      Subsequently, treatment with irisflorentin obviously weakened 
      2,4-dinitro-1-fluorobenzene-induced delayed-type hypersensitivity. These findings 
      suggest new insights into the role of irisflorentin as an immunotherapeutic 
      adjuvant through its capability to modulate the properties of DCs.
FAU - Fu, Ru-Huei
AU  - Fu RH
AD  - Graduate Institute of Immunology, China Medical University, Taichung, Taiwan.
FAU - Tsai, Chia-Wen
AU  - Tsai CW
FAU - Tsai, Rong-Tzong
AU  - Tsai RT
FAU - Liu, Shih-Ping
AU  - Liu SP
FAU - Chan, Tzu-Min
AU  - Chan TM
FAU - Ho, Yu-Chen
AU  - Ho YC
FAU - Lin, Hsin-Lien
AU  - Lin HL
FAU - Chen, Yue-Mi
AU  - Chen YM
FAU - Hung, Huey-Shan
AU  - Hung HS
FAU - Chiu, Shao-Chih
AU  - Chiu SC
FAU - Tsai, Chang-Hai
AU  - Tsai CH
FAU - Wang, Yu-Chi
AU  - Wang YC
FAU - Shyu, Woei-Cherng
AU  - Shyu WC
FAU - Lin, Shinn-Zong
AU  - Lin SZ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150204
PL  - United States
TA  - Cell Transplant
JT  - Cell transplantation
JID - 9208854
RN  - 0 (B7-2 Antigen)
RN  - 0 (CD40 Antigens)
RN  - 0 (Cytokines)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Isoflavones)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (irisflorentin)
RN  - EC 2.7.11.10 (I-kappa B Kinase)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - B7-2 Antigen/metabolism
MH  - Bone Marrow Cells/cytology
MH  - CD40 Antigens/metabolism
MH  - Cytokines/metabolism
MH  - Dendritic Cells/cytology/*drug effects/metabolism
MH  - Dermatitis, Contact/drug therapy/metabolism/pathology
MH  - Histocompatibility Antigens Class II/metabolism
MH  - I-kappa B Kinase/metabolism
MH  - Iridaceae/chemistry/metabolism
MH  - Isoflavones/chemistry/*pharmacology/therapeutic use
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Male
MH  - Medicine, Chinese Traditional
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Phosphorylation/drug effects
MH  - Plant Roots/chemistry/metabolism
MH  - Transcription Factor RelA/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2015/02/06 06:00
MHDA- 2015/12/29 06:00
CRDT- 2015/02/06 06:00
PHST- 2015/02/06 06:00 [entrez]
PHST- 2015/02/06 06:00 [pubmed]
PHST- 2015/12/29 06:00 [medline]
AID - content-CT-2539_Fu_et_al [pii]
AID - 10.3727/096368915X687002 [doi]
PST - ppublish
SO  - Cell Transplant. 2015;24(3):573-88. doi: 10.3727/096368915X687002. Epub 2015 Feb 
      4.